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Biology > TOPIC 6 MARK SCHEME SHIT > Flashcards

TOPIC 6 MARK SCHEME SHIT Flashcards

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1
Q

Explain the banding pattern of a sarcomere (3)

A
  1. Light/I band only actin
  2. H zone only myosin
  3. Darkest/overlapping region actin AND myosin
    • IGNORE REFERENCES TO A BAND
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2
Q

Explain how a decrease in the concentration of calcium ions within muscle tissues could cause a decrease in the force of muscle contraction (3)

A
  1. Less/No tropomyosin moved from binding site/Shape of tropomyosin not changed so binding site not exposed/available
  2. Fewer/No actinomyosin bridges formed
  3. Myosin head doesn’t move/Myosin doesn’t pull actin filaments
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3
Q

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

A
  1. Store of glucose
  2. For respiration/to provide ATP
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4
Q

During vigorous exercise, the pH of skeletal muscle tissue falls. This fall in pH leads to a reduction in the ability of calcium ions to stimulate muscle contraction. Explain 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
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5
Q

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

A
  1. Calcium ions diffuse into myofibrils from sarcoplasmic reticulum
  2. (Calcium ions) cause movement of tropomyosin (on actin)
  3. (This movement causes) exposure of the binding sites on 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 a new ATP molecule to each myosin head causes myosin heads to detach (from actin sites)
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6
Q

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

A
  1. Breaks/allows binding of myosin to actin/actinomyosin bridge
  2. Provides energy to move myosin head
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7
Q

Suggest an explanation for why the mice who couldn’t produce creatine had less forceful muscle contraction than the mice who could produce creatine. (2)

A
  1. Mutant mice unable to make phosphocreatine/less phosphate available to make ATP
  2. So less energy/so less ATP available for contraction
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8
Q

People who have McArdle’s disease produce less ATP than healthy people. As a result, they are not able to maintain strong muscle contractions during exercise. Use your knowledge of the sliding filament theory to suggest why. (3)

A
  1. ATP is needed for attachment/cross bridges between actin and myosin
  2. ATP needed for movement of myosin heads/pulling of actin
  3. ATP needed for detachment of myosin heads
  4. ATP needed for myosin heads to move back to original position
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9
Q

What is the role of phosphocreatine (PC) in providing energy during muscle contraction?

A
  1. Phosphocreatine provides phosphate/phosphorylase’s
  2. To make ATP
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10
Q

Use your knowledge of fast muscle fibres to explain why time for phosphocreatine to be reformed after muscle contraction increases with age. (4)

A
  1. Fast muscle fibres used for rapid/brief/powerful/strong contractions
  2. Phosphocreatine used up rapidly during contraction/to make ATP
  3. As people get older, slower metabolic rate/slower ATP production/slower respiration
  4. ATP used to reform phosphocreatine
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11
Q

If myosin molecules are unable to bind to other myosin molecules, this prevents muscle contractions. Suggest why. (3)

A
  1. Can’t form myosin FILAMENTS
  2. Can’t pull/can’t move actin/slide actin past
  3. Myosin moves/if attached doesn’t move
  4. Can’t move actin towards each other/middle of sarcomere/between myosin/can’t shorten sarcomere/can’t pull Z lines together
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12
Q

Explain why both slow and fast muscle fibres contain ATPase (2)

A
  1. Splitting/breakdown/hydrolysis of ATP
  2. Contraction requires energy/ATP
  3. Use of ATP by MYOSIN
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13
Q

Mitochondrial disease (MD) often causes muscle weakness. Use your knowledge of respiration and muscle contraction to suggest explanations for this effect of MD (3)

A
  1. Reduction in ATP production by aerobic respiration
  2. Less force generated because fewer actin and myosin interactions in muscle
  3. Fatigue caused by lactate from anaerobic respiration
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14
Q

Complete achromatopsia is caused by having only rods and no functional cone cells. Explain why people with this condition have difficulty in seeing detail (3)

A
  1. Only rods/no (functional) cones
  2. Cones are connected to a single neurone/several rods connected to a single neurone
  3. (Cones) separate (sets of) impulses to brain/(rods) single (set of) impulse/s to brain
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15
Q

Explain why trained mice were able to exercise for a longer time period than control mice (3)

A
  1. More ATP produced
  2. Anaerobic respiration delayed
  3. Less/no lactate
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16
Q

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

A
  1. Higher conc of K+ inside AND higher conc of Na+ outside (the neurone)
  2. (Membrane) more permeable to K+ (leaving than Na+ entering)
  3. Na+ (actively) transported out and K+ in
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17
Q

Explain why speed of transmission of impulses is faster along a myelinated axon than 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)
18
Q

A scientist added a respiratory inhibitor to a neurone. The resting potential changed from -70 mV to 0 mV. Explain why (3)

A
  1. No/less ATP produced
  2. No/less active transport OR Na/K pump inhibited
  3. Electrochemical gradient not maintained OR (Facilitated) diffusion of ions causes change to 0 mV OR (Results in) same concentration of (sodium and potassium) ions (either side of the membrane) OR No net movement of (sodium and potassium) ions
19
Q

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

A
  1. Depolarisation of presynaptic MEMBRANE
  2. Calcium channels open and calcium ions enter (synaptic knob)
  3. (Calcium ions cause) synaptic vesicles to fuse with presynaptic membrane AND release acetylcholine
  4. Acetylcholine/neurotransmitter DIFFUSES across (synaptic cleft)
  5. (Acetylcholine attaches) to RECEPTORS on the postsynaptic MEMBRANE
  6. Sodium IONS enter (postsynaptic neurone) leading to depolarisation
20
Q

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

A
  1. (Inside of postsynaptic) neurone becomes more negative/hyperpolarisation
  2. More sodium ions required (to reach threshold)/not enough sodium ions enter (to reach threshold)
  3. For depolarisation/action potential
21
Q

Use your knowledge of how myosin and actin interact to suggest how the myosin molecule moves the mitochondrion towards the presynaptic membrane (2) DO NOT INCLUDE CALCIUM IONS AND TROPOMYOSIN

A
  1. Myosin head attaches to actin AND bends/performs power stroke
  2. Pulls mitochondria past/along the ACTIN
22
Q

Explain how lower temps lead to slower nerve impulse conduction (2)

A
  1. Slower diffusion
  2. Of ions
23
Q

The fovea of an eagle has a high density of cones. An eagle focuses the image of its prey onto the fovea. Explain how the fovea enables an eagle to see its prey in detail. DO NOT REFER TO COLOUR VISION (3)

A
  1. High (visual) ACUITY
  2. (Each) cone is connected to a single neurone
  3. (Cones send) separate (sets of) impulses to the brain
24
Q

The retina of an owl has a high density of rod cells. Explain how this enables an owl to hunt its prey at night. DO NOT REFER TO RHODOPSIN (3)

A
  1. High (visual) SENSITIVITY
  2. Several rods connected to a single neurone
  3. Enough (neuro)transmitter to reach/overcome threshold / SPATIAL summation to reach/overcome threshold
25
Q

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

A
  1. Affects/damages BASEMENT MEMBRANE
  2. Proteins can pass into the (glomerular) filtrate/tubule
26
Q

Describe how ultrafiltration occurs in the glomerulus (5)

A
  1. High blood/hydrostatic pressure
  2. TWO NAMED small substances pass out eg. water, glucose, ions, urea
  3. (Through small) gaps/pores/fenestrations in (capillary) endothelium/presence of podocytes
  4. (And) through (capillary) basement membrane
  5. Protein too large to go through/large so stays behind
27
Q

Explain why concentration of urine increases as thickness of the medulla increases (3)

A
  1. Thicker medulla means longer loop of Henle
  2. (Longer loop of Henle means) INCREASE in Na+ concentration/Na+ gradient maintained for LONGER (in medulla)
  3. Water potential gradient maintained (for longer), SO more water (re)absorbed (from loop and collecting duct)
28
Q

A drug inhibits the absorption of Na+ and Cl- from the filtrate produced in the nephrons. Explain how the drug causes an increase in volume of urine produced (3)

A
  1. WP of filtrate/tubule decreased
  2. Less water (reabsorbed) by OSMOSIS (from filtrate/tubule) - accept more water absorbed by OSMOSIS into filtrate/tubule
  3. Collecting duct (is where osmosis occurs) - accept proximal convoluted tubule or distal or LoH
29
Q

Explain why concentration of filtrate in the tubule increases at first then decreases in the loop of Henle (3)

A
  1. Concentration rises in descending limb because sodium ions enter AND water lost
  2. Concentration falls in ascending limb because sodium ions (and chloride ions) actively removed
  3. But water remains (in ascending limb) because its walls are impermeable (to water)
30
Q

Stimulation of osmoreceptors can lead to ADH secretion. Describe and explain how ADH secretion affects 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
31
Q

Explain why glucose is found in the urine of a person with untreated diabetes (3)

A
  1. High CONCENTRATION of glucose in blood/filtrate
  2. Not all glucose is (re)absorbed at the PROXIMAL CONVOLUTED TUBULE
  3. CARRIER/CO-TRANSPORT PROTEINS are working at a maximum rate/are saturated
32
Q

Describe the role of glucagon in gluconeogenesis. DO NOT INCLUDE SECOND MESSENGER MODEL (2)

A
  1. (Attaches to receptors on target cells) and activates/stimulates enzymes
  2. Glycerol/amino acids/fatty acids into glucose
33
Q

Explain how increasing a cell’s sensitivity to insulin will lower the blood glucose concentration (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/activates enzymes for glycogenesis
34
Q

Explain how inhibiting adenylate cyclase may help lower blood glucose concentration (3)

A
  1. Less/no ATP converted to cAMP
  2. Less/no kinase activated
  3. Less/no glycogen converted to glucose OR less/no glycogenolysis
35
Q

Explain how lack of insulin affects re absorption of glucose in the kidneys of a person who doesn’t secrete insulin (4)

A
  1. High concentration of glucose in blood
  2. High concentration in tubule/filtrate
  3. Reabsorbed by facilitated diffusion/active transport
  4. Requires proteins/carriers
  5. These are working at maximum rate/are saturated
  6. Not all glucose is reabsorbed/some lost in urine
36
Q

Some desert mammals have long loops of Henle and secrete large amounts of ADH. Explain how these two features are adaptations to living in desert conditions. (6)

A

2 marks for general principle:
1. More water (from filtrate) reabsorbed/returned to blood/less lost in urine
2. By osmosis
3. From collecting duct/from end of distal convoluted tubule

2 marks for loop:
1. Sodium/chloride ions absorbed from filtrate in ascending limb
2. Gradient established in medulla/concentration of ions increases down medulla

2 marks for ADH:
1. Acts on collecting duct/DCT
2. Makes cells more permeable/insets aquaporins in plasma membranes

37
Q

Describe how urea is removed from the blood (2)

A
  1. Hydrostatic pressure
  2. Causes ultrafiltration at Bowman’s capsule/glomerulus/renal capsule
  3. Through basement membrane
  4. Enabled because urea is a small molecule
38
Q

Explain how urea in concentrated in the filtrate (3)

A
  1. Reabsorption of water / by osmosis
  2. At the PCT / descending LoH / DCT / CD
  3. Active transport of ions/glucose creates gradient (in context)

Ignore references to facilitated diffusion or to selective reabsorption

39
Q

Advantages of simple reflexes (5)

A
  1. Rapid
  2. Protect against damage to body tissues
  3. Don’t have to be learnt
  4. Help escape from predators
  5. Enable homeostatic control
40
Q

Explain how formation of glycogen in liver cells leads to lowering of blood glucose concentration (2)

A
  1. Glucose concentration in cell/liver falls below that in blood (plasma) which creates/maintains glucose conc/diffusion gradient
  2. Glucose enters cell/leaves blood by facilitated diffusion/via carrier protein/channel protein
41
Q

Adrenaline binds to receptors in the plasma membrane of liver cells. Explain how this causes the blood glucose concentration to increase (2)

A
  1. ADENYLATE CYCLASE activated/cAMP produced/second messenger produced
  2. Activates enzyme(s) (in cell so) glycogenolysis/gluconeogenesis occurs/glycogenesis inhibited
42
Q

Explain why a myelinated axon conducts impulses faster than a non-myelinated one (3)

A
  1. Action potential/depolarisation only at nodes
  2. Nerve impulse jumps from node to node/saltatory
  3. Action potential/impulse doesn’t travel along whole length

Biology (42 decks)

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