Topic 6 Exam Questions: Organisms Respond To Changes In Environments Flashcards

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1
Q

6.1 Control of Heart Rate

Give two safety precautions that should be followed when dissecting a heart. (1)

A

Any two:
Use sharp scalpel/scissors
Wash hands/wear gloves
Disinfect bench/equipment
Cover any cuts
Cut away from self/others/on a hard surface
Safe disposal

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2
Q

6.1 Control of Heart Rate

Explain how the (left) atrioventricular valve maintains a unidirectional flow of blood. (2)

A
  1. Pressure in (left) atrium is higher than in ventricle causing valve to open
    OR (when) pressure above valve is higher than below valve it opens
  2. Pressure in (left) ventricle is higher than in atrium causing valve to close
    OR (when) pressure in below valve is higher than above valve it closes
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3
Q

6.1 Control of Heart Rate

Excessive causes an increase in heart rate. Describe the role of receptors and of the nervous system in this process. (4)

A
  1. Chemoreceptors detect roses in CO2/H+/acidity/carbonic acid/fall in pH
    OR barrio/pressure receptors detect rise in blood pressure
  2. Send impulses to cardiac centre/medulla
  3. More impulses to SAN
  4. By sympathetic (nervous system for chemoreceptors/CO2)
    OR by parasympathetic (nervous stem for baro/pressure receptors/blood pressure)
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4
Q

6.1 Control of Heart Rate

When the heart beats, both ventricle contract at the same time. Explain how this odd coordinated in the heat after initiation of the heartbeat y the SAN. (2)

A
  1. Electrical activity only through Bundle of His/AVN
  2. Wave of electrical activity passes over/through both ventricle at the same time
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5
Q

6.1 Control of Heart Rate

Damage to the myelin sheath of neurones can cause muscular paralysis. Explain how. (3)

A
  1. Saltatory conduction OR (nerve) impulses/depolarisation/ions pass to neurones OR depolarisation occurs along whole length (of axon)
  2. (nerve) impulses showed/stopped
  3. (Refers to) neuromuscular junction OR sarcolemma
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6
Q

6.1 Control of Heart Rate

Suggest and explain how heart rate irregularities can occur with certain syndromes. (3)

A
  1. Slower/fewer impulses along sympathetic/parasympathetic (pathway/neurons)
  2. (Impulses) from cardiac centre OR (impulses) from medulla
  3. To SAN
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7
Q

6.1 Receptors

Explain how the fovea (containing a high density of cones) of an eagle’s eye allows it to see is prey in detail. (3)

A
  1. High (visual) acuity
  2. (Each) cone is connected to a single neurone
  3. (Cones send) separate (sets of) impulses to brain
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8
Q

6.1 Receptors

The retina of an owl has high density of Rod cells. Explain how this enables an owl to hunt at night. (3)

A
  1. High (visual) sensitivity
  2. Several rods connected to a single neurone
  3. Enough (neuro) transmitter to reach/overcome threshold
    OR spatial summation to reach/overcome threshold
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9
Q

6.1 Receptors

Explain how the resting potential of -70mV is maintained in the sensory neurone when no pressure is applied. (2)

A
  1. Membrane more permeable to potassium ions and less permeable to sodium ions
  2. Sodium ions actively transported/pumped out and pain ions in
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10
Q

6.1 Receptors

Explain how applying pressure to the Pacinian corpuscle produces changes in membrane potential. (3)

A
  1. (Pressure causes) membrane/lamellae to become deformed/stretched
  2. Sodium ion channels in membrane open and sodium ions move in
  3. Greater pressure more channels open/sodium ions enter
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11
Q

6.1 Receptors

Explain why the membrane potential would be the same regardless if medium or heavy pressure was applied to the finger tip. (2)

A
  1. Threshold has been reached
  2. (Threshold or above) causes maximal response/all or nothing principle
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12
Q

6.1 Receptors

Multiple sclerosis is a disease where parts of the myelin sheaths surrounding neurones are destroyed. Explain how this results in slower responses to stimuli. (2)

A
  1. Less/no saltatory conduction/action potential/impulses unable to ‘jump’ from node to node
  2. More depolarisation over length/area of membranes
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13
Q

6.1 - Survival and Response

In an investigation into the effect of IAA on growth of seedlings. Explain why the student removed the spot top from each seedling. (2)

A
  1. Tip produces IAA
  2. Affects conc of IAA
    OR affects (shoot) length/growth/elongation
  3. Mitosis/division occurs in shoot tips
  4. Affects (shoot) length/grout/elongation
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14
Q

6.1- Survival and Response

Suggest two advantages of simple reflexes (2)

A
  1. Rapid
  2. Protect against damage to body tissues
  3. Do not have to be learnt
  4. Help escape from predators
  5. Enable homeostatic control
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15
Q

6.2 - Nervous Coordination

Explain how a resting potential is maintained across the axon membrane in a neurone (3)

A
  1. Higher conc of potassium ions inside AND higher conc of sodium ions outside (the neurone) OR Potassium ions DIFFUSE out OR Sodium ions DIFFUSE in
  2. (Membrane) more permeable to potassium ions ( leaving than sodium ions entering)
  3. Sodium ions (actively) transported out and potassium ions in
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16
Q

6.2 - Nervous Coordination

Explain why the speed of transmission of impulses is faster along a myelinated axon then along a non-myelinated axon. (3)

A
  1. Myelination provides (electrical) insulation
  2. (In myelinated) saltatory (conduction) OR (in myelinated) depolarisation at nodes (of Ranvier)
  3. In non-myelinated depolarisation occurs along whole/length (of axon)
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17
Q

6.2 - Nervous Coordination

A scientists investigated the effect of inhibitors . She added a respiratory inhibitor to a neurone. The resting potential of the neurone charged from-70mV to 0mV. Explain why. (3)

A
  1. No/less ATP produced
  2. No/less ACTIVE transport OR sodium/potassium pumping inhibited
  3. Electrochemical Gradient not maintained OR (facilitated) division of ions causes change to 0 mV OR (Results in) same conc of (sodium and potassium) ions (either side of membrane) OR no net movement of (sodium and potassium ions)
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18
Q

6.2 - Nervous Coordination

Describe the sequence of events involved in transmission across a cholinergic synapse. (Do not include details on the breakdown of acetylcholine) (5)

A
  1. Depolarisation of presynaptic MEMBRANE
  2. Calcium channels open and calcium IONS enter (synaptic knob)
  3. (Calcium ions cause) synaptic vesicles move to/fuse with presynaptic membrane AND release acetylcholine/neurotransmitter
  4. Acetylcholine/Neurotransmitter DIFFUSES across (synaptic cleft)
  5. (Acetylcholine attaches) to RECEPTOR on the post synaptic MEMBRANE
  6. Sodium IONS enter (postsynaptic neurone) leading to depolarisation
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19
Q

6.2 - Nervous Coordination

Dopamine stimulates the production. Of nerve impulses in postsynaptic neurone. Describe how. (3)

A
  1. (Dopamine) DIFFUSES across (synapse)
  2. Attaches to RECEPTORS on POSTSYNAPTIC MEMBRANE
  3. Stimulates entry of sodium IONS AND depolarisation/action potential
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20
Q

6.2 - Nervous Coordination

Endorphins (which stimulate release of dopamine for pain relief) attach to opioid receptors on presynaptic neurones that release dopamine. Morphine is a drug that has a similar structure to endorphins and can provide pain relief. Explain how (2)

A
  1. Morphine attaches to OPIOID receptors
  2. (More) dopamine released (to provide pain relief)
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21
Q

6.2 - Nervous Coordination

GABA is a neurotransmitter released in stone inhibitory synapses in the brain. GABA caused negatively charged chloride ions to enter postsynaptic neurones. Explain how this inhibits postsynaptic neurone. (3)

A
  1. (Inside of postsynaptic) neurone becomes more negatively/hyperpolarisation/inhibitory postsynaptic potential
  2. More sodium ions required (to reach threshold) OR not enough sodium ions enter (to reach threshold)
  3. For depolarisation/action potential
22
Q

6.2 - Nervous Coordination

When a nerve impulse arrives at a synapse, it causes the release of neurotransmitter from vesicles in the presynaptic knob. Describe how. (3)

A
  1. (Nerve impulse/depolarisation of membrane) causes Ca2+ channel (proteins) to open
  2. Ca2+ enter by (facilitated) diffusion
  3. Causes (synaptic) vesicles to fuse with (presynaptic) membrane
23
Q

6.2 - Nervous Coordination

Use your knowledge of myosin and actin to suggest how a molecule of myosin moves the mitochondrion towards the presynaptic membrane. (2)

A
  1. Myosin hear attaches to action and Brenda/performs powerstroke
  2. (This) pulls mitochondria past/along the actin
  3. Other/next myosin head attaches to actin (and bends/performs powerstroke)
24
Q

6.2 - Nervous Coordination

Suggest and explain one advantage of movement of mitochondria when nerve impulse arrives to wards the presynaptic membrane (2)

A
  1. (Mitochondria) supply (additional) ATP/energy
  2. To move vesicles/for active transport of ions/for myosin to move past actin OR re-synthesis/re absorption of neurotransmitter
25
Q

6.3 - Contraction of Skeletal Muscles

Explain the banding pattern of a sarcomere (3)

A
  1. I band only actin
  2. H zone/band only myosin
  3. Overlapping region actin and myosin
26
Q

6.3 - Contraction of Skeletal Muscles

An increase in the conc of Pi prevents release of calcium ions within muscle tissue. Explain how a decrease in the concentration of calcium ions within muscle tissues could cause a decrease in force of muscle contraction. (3)

A
  1. (Less/No) TROPOMYOSIN moved from binding site OR shape of TROPOMYOSIN not changed so binding site not exposed/available
  2. (Fewer/No) actinomyosin bridges formed
  3. Myosin head does not move OR Myosin does not pull actin (filaments) OR (less/no) ATP (hydrol)ASE (activation)
27
Q

6.3 - Contraction of Skeletal Muscles

In muscles, pyruvate is converted to lactate during prolonged exercise. Explain why converting private to lactate slows the continued production of ATP by anaerobic respiration. (2)

A
  1. Regenerates/produces NAD OR oxidises reduced NAD
  2. (So) glycolysis continues
28
Q

6.3 - Contraction of Skeletal Muscles

The scientist compared the length of time that the control mice and the trained mice could carry out prolonged exercise. The trained mice were able to exercise longer than the control mice. Explain why. (3)

A
  1. (More aerobic respiration) produces more ATP
  2. anaerobic respiration delayed
  3. Less or no lactate
29
Q

6.3 - Contraction of Skeletal Muscles

Explain the role of glycogen granules present in the skeletal muscle. (2)

A
  1. As a style of glucose OR to be hydrolysed to glucose
  2. For respiration/to provide ATP
30
Q

6.3 - Contraction of Skeletal Muscles

During vigorous exercise, the pH of skeletal muscle tissue falls. This fall on pH leads to a reduction in the ability of calcium ions to stimulate muscle contraction. Suggest how. (3)

A
  1. Low pH changes shape of calcium ion receptors
  2. Fewer calcium ions bind to tropomyosin
  3. Fewer Tropomyosin molecules move away
  4. Fewer binding sites on actin revealed
  5. Fewer cross-bridges can form OR fewer myosin heads can bind
31
Q

6.3 - Contraction of Skeletal Muscles

Describe the roles of calcium ions and ATP in the contraction of a myofibril (5)

A
  1. Calcium ions diffuse into myosotis from (sarcoplasmic) reticulum
  2. (Calcium ions) cause movement of Tropomyosin (on actin)
  3. (This movement causes) exposure of binding sites on the actin
  4. Myosin heads attach to binding sites on actin
  5. Hydrolysis of ATP (on myosin heads) causes myosin heads to bend
  6. (Bending) pulling actin molecules
  7. Attachment of new ATP molecule to wash myosin head causes myosin heads to detach (from actin sites )
32
Q

6.3 - Contraction of Skeletal Muscles

ATP is an energy source used in many cell processes. Give two ways in which ATP is a suitable energy source for cells to use (2)

A
  1. Releases relatively small amount of energy/little energy is lost as heat
  2. Release energy instantaneously
  3. Phosphorylates other compounds, making them more reactive
  4. Can be rapidly re-synthesised
  5. Is not lost from/does not leave cells
33
Q

6.3 - Contraction of Skeletal Muscles

What is the role of ATPB in myofibril contraction? (2)

A
  1. (Reaction with ATP) breaks/allows binding of myosin to actin/actinomyosin bridge
  2. Provides energy to move myosin head
34
Q

6.4 - Control of blood glucose concentration

Explain why the change in amino acid sequence of insulin prevents it from binding to its receptor. (2)

A
  1. Changes TERTIARY structure
  2. No longer COMPLEMENTARY (to receptor)
35
Q

6.4 - Control of blood glucose concentration

Using your knowledge of the kidney, explain why glucose is found in the urine of a person with untreated diabetes. (3)

A
  1. High CONC of glucose in blood/ filtrate
  2. Not all the glucose is (re)absorbed at the PROXIMAL CONVOLUTED TUBULE
  3. CARRIER/CO-TRANSPORT PROTEINS are working at maximum rate OR carrier proteins are saturated
36
Q

6.4 - Control of blood glucose concentration

Describe the role of glucagon in gluconeogenesis (2)

A
  1. (Attaches to receptors on target cells and) activates/stimulates enzymes
  2. Glycerol/amino acids/fatty acids into glucose
37
Q

6.4 - Control of blood glucose concentration

Explain how increasing a cell’s sensitivity to insulin will lower the blood glucose conc (2)

A
  1. (More) insulin binds to receptors
  2. (Stimulates) uptake of glucose by channel/transport PROTEINS OR activates enzymes which convert glucose to glycogen
38
Q

6.4 - Control of blood glucose concentration

Explain how inhibiting adenylate cycle may help to lower the blood glucose conc. (3)

A
  1. Less/no ATP is converted to cyclic AMP/cAMP
  2. Less/no kinase is activated
  3. Less/no glycogen is converted to glucose ORB less/no glycogenolysis
39
Q

6.4 - Control of blood glucose concentration

People with type 1 diabetes can be given pancreas transplants but people with type 2 can’t. Give two reasons why Pancras transplants are not used for the treatment of type 2 diabetes (2)

A
  1. (Usually) type 2 produces insulin
  2. Cells/receptors less sensitive/responsive (to insulin) OR faulty (insulin) receptors
  3. (Treated/ controlled by) diet/exercise
40
Q

6.4 - Control of blood glucose concentration

Give two ways in which people with type 1 diabetes control their blood glucose conc. (2)

A
  1. Treat with insulin (injections/infusion)
  2. Control diet/sugar intake
41
Q

6.4 control of blood water potential

Alport syndrome (AS) is an inherited disorder that affects kidney glomeruli of both men and women. Affected have proteinuria (high quantities of protein in urine) Suggest how AS could cause proteinuria. (2)

A
  1. Affects/damages BASEMENT MEMBRANE OR more protein channels/carriers in BASEMENT MEMBRANE
  2. Protein can pass into the (glomerular) filtrate tubule
42
Q

6.4 control of blood water potential

Describe how ultrafiltration occurs in the glomerulus (3)

A
  1. High blood/hydrostatic pressure
  2. Two named small substances pass out e.g water, glucose, ions, urea
  3. (Through small) gaps/pores/fenestrations in (capillary) endothelium
  4. (And) through (capillary) basement membrane
43
Q

6.4 control of blood water potential

Furosemide is sometimes used to treat high blood pressure. Suggest how (1)

A

Lower VOLUME of blood

44
Q

6.4 control of blood water potential

Furosemide inhibitors the absorption of sodium and chloride ions from filtrate produced in the nephrons. Explain how it causes an increase in the volume of urine produced. (3)

A
  1. Water potential of filtrate/tubule decreased
  2. Less water (reabsorbed) by OSMOSIS (from filtrate/tubule)
  3. Collecting duct (is where osmosis occurs)
45
Q

6.4 control of blood water potential

Give the location of osmoreceptors in a mammal. (1)

A

Hypothalamus

46
Q

6.4 control of blood water potential

When a person is dehydrated, the cell volume of an osmoreceptor decreases. Explain why. (2)

A
  1. Water potential of blood will decrease
  2. Water moves from ismoreceptor into blood by osmosis
47
Q

6.4 control of blood water potential

Stimulation of osmoreceptors can lead to secretion of ADH. Describe and explain how the secretion of ADH affects the urine produced by the kidneys. (4)

A
  1. Permeability of membrane/cells (to water) is increased
  2. More water absorbed from /leaves distal tubule/ collecting duct
  3. Smaller volume of urine
  4. Urine becomes more concentrated
48
Q

6.4 control of blood water potential

Apart from age and gender, give two factors that could affect the conc of Creatinine in the blood. (1)

A
  1. Muscle/body mass
  2. Ethnicity
  3. Exercise
  4. Kidney disease
49
Q

6.4 - Homeostasis

The acidic pH conditions created by osteoclasts cause the inactive form of the protein osteocalcin to change into the active form of osteocalcin. Suggest how. (2)

A
  1. (Change in pH) changes/breaks ionic/hydrogen bonds
  2. Changes in tertiary structure
50
Q

6.4 - Homeostasis

Binding of insulin leads to an increase in the rate of respiration in cells such as osteoblasts. Explosion how. (2)

A
  1. (Insulin) leads to more transport proteins/channel (proteins)/ carrier (proteins) for glucose
  2. More glucose (for respiration/glycolysis) enters cell
51
Q

6.4 - Homeostasis

The regulation of the formation of helper T cells by Interferon gamma is an example of positive feedback. Explain why it is an example of positive feedback. (2)

A
  1. Causes more helper T cells to form
  2. (So) more interferon (gamma) production (by helper Tcells)