Organisms respond to changes in their internal and external environments Flashcards
(114 cards)
1
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What is homeostasis
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Maintenance of a stable internal environment within restricted limits by physiological control systems
2
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High temperature means..
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H bonds in tertiary structure break, enzymes denature, active sites change shape and substrates can’t bind, fewer ES complexes
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Low temperature means..
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Not enough kinetic energy, fewer ES complexes
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Above/below optimal pH means..
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Ionic/Hydrogen bonds in tertiary structure break, enzymes denature, active sites change shape and substrates can’t bind, fewer ES complexes
5
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Negative feedback systems
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-Receptors detect change from optimum
-Effectors respond to counteract change
-Returning levels to optimum
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Positive feedback systems
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-Receptors detect change from normal
-Effectors respond to amplify change
-Producing a greater deviation from normal
7
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Glycogenesis converts
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glucose→glycogen
8
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Glycogenolysis converts
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glycogen→glucose
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Gluconeogenesis converts
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amino acids/glycerol→glucose
10
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When is insulin secreted
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When beta cells in islets of Langerhans in pancreas detect high blood glucose concentration
11
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Action of insulin
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Attaches to specific receptors on cell surface membranes of target cells→more glucose channel proteins join cell surface membranes→ increases permeability to glucose→ more glucose enters by facilitated diffusion
-Enzymes involved in glycogenesis→ lowers glucose conc in cells → glucose enters cells by facilitated diffusion. down conc gradient
12
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When is glucagon secreted
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When alpha cells in islets of Langerhans in pancreas detect blood glucose conc is. too low
13
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Action of Glucagon
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Attaches to specific receptors on cell surface membrane of target cells→activates enzymes involved in glycogenolysis→activates enzymes involved in gluconeogensis
14
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When is adrenaline secreted
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Fear, stress, exercise
15
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Role of Adrenaline
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Attaches to specific receptors on cell surface membrane of target cells→activates enzymes involved in glycogenolysis
conc gradient- glucose leaves cells and enters blood by fd
16
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Second messenger model- adrenaline and glucagon
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First messenger (adrenaline and glucagon) attach to to specific receptors which:
Activate enzymes adenylate cyclase→converts many ATP to many cyclic AMP→cAMP acts as second messenger → activates protein kinase enzymes→activates enzymes for glycogenolysis
17
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Advantage of second messenger model
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Amplifies signal from hormone as each hormone can stimulate production of many molecules of a second messenger, which can activate many enzymes for rapid increase in glucose
18
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Causes of Type 1 Diabetes
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-Beta cells in islets of langerhans in pancreas produce insufficient insulin
-Normally develops in childhood due to an autoimmune response destroying beta cells in islets of langerhans
19
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Control by insulin-Type 1
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Injections of insulin. (not orally as protein is digested)
Blood glucose concentration monitored with biosensors, dose of insulin matches to glucose intake
20
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Control by diet manipulation-Type 1
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Eating regularly, control carbohydrate intake to avoid sudden rise in glucose
21
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Causes of Type 2 Diabetes
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Receptor loses responsiveness to insulin, fewer glucose transport proteins, less uptake of glucose, less conversion of glucose to glycogen
22
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Control by insulin-Type 2
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Not normally treated this way, uses drugs which target insulin receptors to increase their sensitivity- more glucose uptake
23
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Control by diet manipulation-Type 2
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-Reduced sugar intake, less absorbed
-Reduced fat intake, less glycerol to glucose
-More exercise, uses glucose by respiration
-Weight loss- More sensitivity of receptors to insulin
24
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Effects of hypoglycaemia
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Not enough glucose for respiration→ less ATP produced→ active transport can’t occur → cell death
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Effects of 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
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Function of Bowman's/ renal capsule
Formation of glomerular filtrate
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Function of proximal convoluted tubule
Reabsorption of water and glucose
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Function of Loop of Henle
Maintenance of a gradient of sodium ions in the medulla
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Function of distal convoluted tubule and collecting duct
Reabsorption of water
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How is glomerular filtrate formed
-High hydrostatic pressure in glomerulus (as the diameter of the afferent arteriole is wider than the efferent arteriole)
-Small substances are forced into glomerular filtrate
-Filtered by:
→pores between capillary endothelial cells
→capillary basement membrane
→podocytes
-Large proteins/blood cells remain in the blood
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How is glucose reabsorbed by the proximal convoluted tube
-Sodium ions actively transported out of epithelial cells to capillary→moved by facilitated diffusion into epithelial cells down conc. gradient, bringing glucose against its conc gradient → glucose moves into capillary by facilitated diffusion down its conc. gradient
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How is water reabsorbed by the proximal convoluted tube
Glucose in capillaries lowers water potential, so water moves by osmosis down a water potential gradient
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In diabetics, why isn't all glucose reabsorbed
Blood glucose conc too high→ glucose carrier proteins are working at max rate
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How is a gradient of sodium ions maintained in the medulla by the loop of Henie
Ascending limb: Sodium ions actively transport out (filtrate conc decreases) → water remains as impermeable to water→increases conc of sodium ions in medulla, lowering water potential
Descending limb: Water moves out by osmosis then reabsorbed by capillaries (filtrate conc increases) → sodium ions recycled→ diffuses back in
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Importance of maintaining a gradient
Increases concentration of sodium ions further down→so water potential decreases down the medulla→water potential gradient maintained between collecting duct and medulla to maximise reabsorption of water by osmosis from filtrate
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Why do animals needing to conserve water have long loops of Henie
More sodium ions moved out → sodium ion gradient is maintained for longer in. medulla→water potential gradient is maintained for longer and more water can be reabsorbed from collecting duct by osmosis
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How is water reabsorbed by the distal convoluted tubule and collecting ducts
Water moves out of the distal convoluted tubule and collecting duct by osmosis down a water potential gradient, controlled by ADH which increases their permeability
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What is osmoregulation
Control of water potential of the blood
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Function of the hypothalamus
-Contains osmoreceptors- detects blood water potential
-Produces ADH
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Function of posterior pituitary gland
-Secrete ADH into blood due to signal from hypothalamus
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Function of antidiuretic hormone (ADH)
-More secreted when blood water potential is low
-Increases permeability of cells of collecting duct and DCT to water→ increases water reabsorption into blood→ decreases volume and increases conc of urine produced
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How does the body respond to a decrease in water potential
-In the hypothalamus, osmoreceptors detect a decrease in water potential→ produces more ADH
-Posterior pituitary gland secretes more ADH into blood
-ADH attaches to receptors on collecting duct→ increasing permeability of cells to water (aquaporins join cell surface membrane)→so more water reabsorbed from collecting duct by osmosis
-Urine=smaller volume and more concentrated
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How do organisms increase their chance of survival
They respond to stimuli
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What is a stimulus
Change in organisms internal or external environment
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What is tropism
growth of a plant in response to a directional stimulus
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What is the role of growth factors in flowering plants
Specific factors move from growing regions (root/shoot tips) to other tissues where they regulate growth in response to directional stimuli
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How does indoleacetic acid affect cell elongation in roots v shoots
In shoots, high conc of IAA stimulate cell elongation
In roots, high conc. of IAA inhibits cell elongation
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Gravitropism
-Cells in tip of shoot/ root produce IAA
-IAA diffuses down shoot/ root
-IAA moves to lower side of shoot/ root so conc increases
-Shoots bend away from gravity, roots bends towards gravity
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Phototropism
-Cells in tip of shoot/root produce IAA
-IAA diffuses down shoot/root so conc increases
-In shoots this stimulates cell elongation whereas in roots this inhibits cell elongation
-Shoots bend towards light, roots bend away from light
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Taxes response
Directional response.
Movement towards or away from stimulus
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Kineses response
Non directional response.
Speed of movement changes in response to a non directional stimulus.
Intensity is a factor.
E.G. woodlice move faster when drier to raise chance of moving to higher humidity to prevent drying out
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Protective effect of simple reflex
Stimulus →receptor →sensory neurone →relay neurone →motor neurone →effector →response
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Importance of protective effect
-Rapid →only 3 neurones and few synapses (synaptic transmission is slow)
-Autonomic so doesn't have to be learnt by brain
-Protects from harmful stimuli
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How does deformation of stretch mediated sodium ion channel cause generator potential
-Mechanical stimulus (e.g.high pressure)
-Sodium ion channels in membrane open and sodium ions diffuse into sensory neurone
-Greater pressure causes more sodium ion channels to open and more sodium ions to enter
-Causing depolarisation, leading to generator potential
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What does the pacinian corpuscle illustrate?
Receptors respond only to specific stimuli- only responds to mechanical pressure.
Stimulation of a receptor leads to the establishment of a generator potential
When threshold is reached, action potential triggered.
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What are the features of a myelinated motor neurone
-Dendrite
-Axon [myelin sheath (made of Shwann cells), Node of Ranvier in gaps]
-Cell body (soma)
-Axon terminal
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Establishment of a resting potential
-Na+/K+ pump actively transports
-3 Na+ out of axon
-2 K+ into axon
-This creates an electrochemical gradient
-Differential membrane permeability:
-More permeable to K+, moves out by fd
-Less permeable to Na+ (closed channels)
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What happens at resting potential
Inside of axon has a negative charge relative to outside, as there are more positive ions outside compared to inside
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What do changes in permeability lead to
Depolarisation, and the generation of an action potential
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Stimulus
-Na+ channels open; membrane permeability to Na+ increases
-Na+ diffuse into axon down electrochemical gradient (causing depolarisation)
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Depolarisation
-If threshold potential is reached, an action potential is generated:
-As more voltage-gated Na+ channels open (positive feedback effect)
-More Na+ diffuses in rapidly
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Repolarisation
-Voltage-gated Na+ channels close
-Voltage-gated K+ channels open; K+ diffuses out of axon
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Hyperpolarisation
K+ channels slow to close so there's a slight overshoot- too many K+ diffuse out
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Resting potential
Restored by Na+/K+ pump
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All or nothing principle explained
Depolarisation has to exceed threshold potential, for action potential production. Action potentials are always the same magnitude at same potential
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Factor that affects action potential
Bigger stimuli increases frequency of action potentials
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Passage of action potential along non myelinated axon
-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 so adjoining region depolarises
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Passage of action potential along myelinated axon
-Myelination provides electrical insulation
-Depolarisation of axon at nodes of Ranvier only
-Results in saltatory conduction (local currents circuits)
-No need for depolarisation along whole length of axon
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What happens if the myelin sheath is damaged
Slow responses/jerky movement
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What Is an action potential
When the neuron's voltage increases beyond a set point from the resting potential (-70mV) , generating nervous impulse
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What causes increases in voltage aka depolarisation
Neurone membrane becomes more permeable to sodium ions
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Nature and Importance of the refractory period
Ion channels are recovering and don't open, so there's a time delay between action potentials ∴ :
-Actions potentials don't overlap, but pass along as separate impulses
-There's a limit to the frequency at which nerve impulses are transmitted
-Action potentials are unidirectional (only travel in one direction)
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How does axon diameter affect speed of conductance
Bigger diameter so less leakage of ions, less resistance to flow of ions
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How does temperature affect speed of conductance
-Increases rate of movement of ions as more kinetic energy
-Higher rate of respiration due to faster enzyme activity, ATP produced faster and energy released faster (because active transport is faster)
*PROTEINS CAN DENATURE AT V HIGH TEMPS
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Where are rods and cones found
retina
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Rods
More sensitive to light
-Several rods connected to a single neurone
-Spatial summation to reach threshold to generate action potential
Lower visual acuity
-Several rods connected to a single neurone, so they send a single set of impulses to brain (brain can't distinguish between separate sources of light)
Allow monochromatic vision
-1 rod (1 pigment)
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Cones
Less sensitive to light
-Each cone is connected to a single neurone
-No spatial summation
Cones give higher visual acuity
-Each cone connected to a single neurone
-Cones send separate sets of impulses to brain so it can distinguish between separate sources of light
Cones allow colour vision
-3 types of cones (red, green, blue) with different optical pigments (so absorb different wavelengths
-Stimulation of different combinations of cones gives a range of colour perception
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What does myogenic mean (cardiac muscle is myogenic)
Can contract/relax without receiving electrical impulses from nerves
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Role of the sinoatrial node
Acts as a pacemaker and sends out regular waves of electrical impulses across both atria causing right/left atria to contract simultaneously
Waves of electrical activity reaches atrioventricular node
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What prevents waves crossing directly to ventricles
Layer of non conductive tissue
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Where are chemoreceptors and baroreceptors located
In aorta and cartoid arteries
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Role of atrioventricular node
Delays impulse allowing atria to fully contact and empty
Passes waves of electrical activity to 'bundle of His' which conducts wave between ventricles to the apex of the heart, where the bundle branches into smaller fibres of Purkyne tissue
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How are baroreceptors stimulated by low blood pressure
More frequent impulses to medulla, more frequent impulses sent to SAN along sympathetic neurones, more frequent impulses sent from SAN, cardiac muscle contracts more frequently so heart rate increases
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How are baroreceptors stimulated by high blood pressure
More frequent impulses to medulla, more frequent impulses sent to SAN along parasympathetic neurones, less frequent impulses sent from SAN, cardiac muscle contracts less frequently so heart rate decreases
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How are chemoreceptors stimulated by high blood CO2 conc/ low pH
More frequent impulses to medulla, more frequent impulses sent to SAN along sympathetic neurones, more frequent impulses sent from SAN, cardiac muscle contracts more frequently so heart rate increases
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How are chemoreceptors stimulated by low blood CO2 conc/ high pH
More frequent impulses to medulla, more frequent impulses sent to SAN along parasympathetic neurones, less frequent impulses sent from SAN, cardiac muscle contracts less frequently so heart rate decreases
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What happens when action potential reaches the end of a neurone
Neurotransmitters (which are contained in synaptic vesicles in the synaptic knob of the presynaptic neurone) are released into the synaptic cleft. They diffuse across to the postsynaptic membrane and bind to specific receptors.
*Neurotransmitters will either be broken down by enzymes or taken back not presynaptic neurone so response doesn't keep happening.
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What's a synapse and synaptic cleft
Synapse- junction between a neurone and another neurone/an effector cell
Synaptic cleft- Tiny gaps between cells at a synapse
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What happens when neurotransmitters bind to specific receptors
They might trigger an action potential, cause muscles contraction, or cause hormone to be secreted.
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How is a nerve impulse transmitted across a cholinergic synapse
-An action potential arrives at the synaptic knob of the presynaptic neurone
-This stimulates voltage-gated calcium ion channels in the presynaptic neurone to open
-Calcium ions diffuse into the synaptic knob
-The influx of calcium ions cause the synaptic vesicles to move to the presynaptic membrane, they then fuse with the membrane
-The vesicles release the neurotransmitter acetylcholine into the synaptic cleft (exocytosis)
-Acetylcholine diffuses across the synaptic cleft and binds to specific cholinergic receptors on postsynaptic membrane
-Causes sodium ion channels in the postsynaptic neurone to open
-Influx of sodium ions into the postsynaptic membrane causes depolarisation, action potential
generated if threshold is reached
-Acetylcholine is removed from the synaptic cleft so the response doesn't keep happening, broken down by acetylcholinesterase and the products are reabsorbed by presynaptic neurone and used to make more acetylcholine
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Why are the impulses unidirectional
Because the receptors are only on the post synaptic membrane , impulses can only travel in one direction
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Cholinergic synapses v neuromuscular junctions
-Cholinergic synapses; neurone to neurone whereas neuromuscular; neurone to muscle
-Neuromuscular; acetylcholine is always excitatory and never inhibitory, so always triggers action potential
-Neuromuscular junction; post synaptic membrane has more receptors than other synapses.
-Neuromuscular junction; lots of folds on post synaptic membrane which. forms clefts to store enzyme (acetylcholinerase) to break down neurotransmitter
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Excitatory neurotransmitters
Depolarise the postsynaptic membrane, making it fire an action potential when threshold is reached
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Inhibitory neurotransmitters
Hyperpolarise the postsynaptic membrane (making pd more negative), preventing it from fitting an action potential
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Where are neuromuscular junctions
-Synapse between motor neurone and a muscle cell
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What is summation
Addition of a number of impulses converging on a single post-synaptic neurone
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Spatial summation
Many presynaptic neurones share the same synaptic cleft/ post synaptic neurone, and release sufficient neurotransmitters to reach threshold and trigger an action potential
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Temporal summation
One presynaptic neurone releases neurotransmitter many times over a short period. Sufficient neurotransmitter to reach threshold to trigger an action potential
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How do muscles work and where are they
In antagonistic pairs:
-One contracts (agonist); pulls on bone produces a force
-One relaxes (antagonist)
e.g. biceps and triceps
-Attached to bones by tendons
-Ligaments attached from one bone to the other to hold them together
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What are advantages of skeletal muscle being arranged in antagonistic pairs
-Muscles can only contract
-2nd muscles required to reverse movement caused by 1st
-Helps maintain posture
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Gross structure of skeletal muscle
Muscle made up of bundles of muscle fibres (muscle cells) packages together
Muscle cells contain;
-Cell membrane=sarcolemma
-Cytoplasm=sarcoplasm
-Myofibrils made up of actin and myosin
-Shared nuclei
-Lots of endoplasmic reticulum
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Ultrastructure of a myofibril
-Made up many sarcomeres which are made up of partly overlapping myosin (thick, dark A bands ) and actin (thin, light I bands) filaments (proteins)
-A sarcomere contains;
-Ends (z line)
-Middle (A band) and overlap
-H zone (only contains myosin), middle (no overlap)
-M line in the middle
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Muscle contraction- Sliding filament theory
Myosin and actin filaments slide over each other to make sarcomeres contract.
Simultaneous contractions of sarcomeres cause myofibrils and. muscle fibres to contact.
During contraction:
-H zones get shorter
-I (isotropic) bands get shorter
-A (anisotropic) bands stay the same
-Z lines get closer
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Why can myosin filaments move back and forth and what binding sites do they have
Myosin filament have globular heads and are unhinged
Each myosin head has a binding site for actin and a binding site for ATP
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Structure of actin filaments
Actin filaments have binding sites for myosin heads, called action-myosin binding sites
Tropomyosin is found between actin filaments, this helps myofilaments move past each other
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Why cant myofilaments slide pass each other in resting muscles
The actin myosin binding side is blocked by tropomyosin, so the myosin heads can't bind to the actin myosin binding site on the actin filaments
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Name 3 types of muscles in the body and where they are located
Cardiac; exclusively found in heart
Smooth; walls of blood vessels and intestines
Skeletal; attached to incompressible skeleton attached by tendons
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How is muscle contraction stimulated
-Action potential from a motor neurone. stimulates a muscle cell, depolarises sarcomella
-Depolarisation spreads down the T-tubules to the sarcoplasmic reticulum
-Sarcoplasmic reticulum releases Ca2+ into sarcoplasm
-Ca2+ binds to a protein attached to tropomyosin, causing the protein to change shape
-Attached tropomyosin is pulled out of actin-myosin binding site on actin filament
-Exposes binding site, allows myosin head to bind (actin-myosin cross bridge forms)
-Ca2+ activated ATP hydrolase (hydrolyses ATP) to provide energy for contraction
-Energy released from ATP causes myosin head to bend, which pulls the actin filament in a rowing action
-Another ATP. provides energy to break actin-myosin cross bridge, so myosin head detaches from the actin filament after its moved
-Myosin head reattaches to a different binding site further along the actin filament and process is repeated
-Many actin-myosin cross bridges form and break, pulling the actin filament along- shortens sarcomere, contracts muscle
-Cycle continues as long as Ca2+is present.
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What happens when Ca2+ leave their binding sites
-Ca2+ moved by active transport back into the sarcoplasmic reticulum (need ATP)
-Causes tropomyosin molecules to move back and block actin myosin binding sites
-Muscles don't contract as no myosin heads are attached to actin filaments ( no cross bridges)
-Actin filaments slide back to relaxed position, sarcomere lengthens
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How does aerobic respiration produce ATP for muscle reactions
-ATP generated via oxidative phosphorylation in the cells mitochondria
-Aerobic respirations works when there's oxygen so its good for low intensity exercise
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How does anaerobic respiration produce ATP for muscle contraction
-ATP made by glycolysis
-Produces pyruvate which is converted to lactate by lactate fermentation
-Lactate quickly builds up causing muscle fatigue
-Anaerobic is good for short intense exercise
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How does ATP phosphocreatine produce ATP for muscle contraction
-ATP made by phosphorylating ADP
-PCr stored in cells and ATP-PCr system generates ATP rapidly
-PCr runs out after seconds so its used during short intense exercise
-ATP-PCr system is anaerobic and. doesn't form lactate (alactic)
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Slow twitch muscle fibres
-Contract slowly
-Used for posture
-Good for endurance activities
-Works for a long time without getting tired
-Energy released slowly through aerobic respiration, lots of mitochondria and blood vessels supply muscles with oxygen
-Reddish in colour as they're rich in myoglobin (red colour protein that stores oxygen)
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