Flashcards · 9610 · AS Topic 2

Biological systems and disease (AS Level) flashcards

109 cards on AS Topic 2, subtopics 3.2.1 to 3.2.11. Pick a subtopic or study them all.

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3.2.1 The causes of disease: pathogens, lifestyle and genes

Pathogen: An agent of infection, such as a bacterium or virus, that can cause disease.
Two ways pathogens cause disease: Damaging host cells directly, and producing toxins that disrupt cell or tissue function, sometimes far from the infection site.
Toxin: A poisonous chemical produced by a pathogen that disrupts cell or tissue function, sometimes distant from the infection site.
Through which interfaces with the environment can pathogens enter a mammal?: The digestive, reproductive and gas-exchange systems (the skin is a further interface). Name the one that fits the example.
Risk factor: A variable statistically associated with an increased likelihood of disease, without necessarily being proven to cause it.
Correlation: A statistical relationship between two variables; on its own it does not show that one causes the other.
Three steps for interpreting disease-incidence data linked to a lifestyle factor: 1 Describe the pattern, with figures. 2 State the conclusion the data are consistent with (the factor is a risk factor). 3 Name another variable that could explain the pattern, so correlation does not prove cause.
Give an example of disease caused mainly by a toxin, and one caused mainly by cell damage: Toxin: tetanus, whose bacterial toxin affects the nervous system and causes muscle spasms. Cell damage: many viruses, which replicate inside host cells and rupture them.
Lifestyle risk factors associated with coronary heart disease: Smoking, high blood pressure, high blood cholesterol, and a diet high in saturated fat or salt. Changing these can reduce the risk.

3.2.2 Digestion and absorption

Digestion, absorption and assimilation: Digestion: hydrolysis of large molecules by enzymes into smaller ones. Absorption: the products cross the gut wall into the body. Assimilation: absorbed substances become part of cells and tissues.
Digestion of starch: Amylase (from salivary glands and pancreas) hydrolyses starch to maltose. Membrane-bound maltase on ileum epithelial cells hydrolyses maltose to glucose.
Endopeptidases, exopeptidases and dipeptidases: Endopeptidases hydrolyse peptide bonds inside the chain, giving shorter chains. Exopeptidases remove amino acids from the ends. Membrane-bound dipeptidases split dipeptides into two amino acids.
Role of bile salts in lipid digestion: They emulsify lipids into small droplets, increasing the surface area for lipase, and later help form micelles. They are not enzymes and do not digest fat chemically.
Products of lipid digestion by lipase: Triglycerides are hydrolysed to monoglycerides and fatty acids.
How is the ileum adapted for absorption?: Villi and microvilli give a large surface area; a single layer of epithelium gives a short diffusion path; a capillary network keeps gradients steep; epithelial cells have many mitochondria for active transport.
How are glucose and amino acids absorbed in the ileum?: The sodium–potassium pump removes Na⁺ from the epithelial cell into the blood using ATP. Na⁺ enters from the lumen down its gradient through a co-transporter, carrying glucose or an amino acid in against its gradient; it leaves into the blood by facilitated diffusion.
Micelle and chylomicron: Micelle: bile salts with fatty acids and monoglycerides; carries them to the epithelial surface. Chylomicron: triglycerides rebuilt inside the cell, packaged with protein and phospholipid; leaves by exocytosis into a lacteal.
A 60-amino-acid polypeptide is cut by an endopeptidase at three places. How many peptide bonds and fragments remain?: The chain has 59 bonds. Three cuts leave 56 bonds and give 4 fragments.

3.2.3 Cholera

Cause and spread of cholera: The bacterium Vibrio cholerae, usually spread in contaminated water or food. It secretes a toxin in the small intestine.
How does the cholera toxin cause watery diarrhoea?: It increases secretion of chloride ions into the gut lumen; sodium ions follow. The lumen water potential falls below that of the cells and blood, so water moves out by osmosis, causing severe watery diarrhoea and dehydration.
What does an oral rehydration solution (ORS) contain?: Water, glucose and salts including sodium ions.
Why does an oral rehydration solution work?: Glucose and sodium ions are still absorbed from the gut by co-transport, lowering the water potential of the epithelial cells, so water follows them by osmosis.
Why is water alone a poor treatment for cholera dehydration?: It supplies no glucose to drive sodium ion uptake by co-transport, so less water follows by osmosis.
Limitations of oral rehydration solutions: They need clean water, treat the symptom (dehydration) not the infection, and severe cases still need intravenous fluid.
Ethical points for a trial of a new oral rehydration solution: Informed consent (from parents for children), the right to withdraw, no untreated placebo group, ethics committee approval, no exploitation of vulnerable people, and fair access afterwards.
A 50 kg patient loses 500 mL of stool per hour for 10 hours. Volume lost, and as a percentage of body mass (1 L ≈ 1 kg)?: 0.5 L × 10 = 5 L. 5 ÷ 50 × 100 = 10% of body mass.
An ORS contains 75 mmol of glucose per litre. What mass of glucose (Mr 180.16) is in 1.5 litres?: 1.5 × 75 = 112.5 mmol = 0.1125 mol. 0.1125 × 180.16 = 20.3 g.

3.2.4 HIV as an example of a human disease caused by a virus

Why are viruses described as acellular and non-living?: Acellular: not made of cells; no cytoplasm, ribosomes or metabolism of their own. Non-living: they cannot respire, grow or reproduce outside a host cell.
Structure of HIV, from the outside in: Lipid envelope (from the host cell membrane) carrying glycoproteins; protein capsid; inside the capsid, two copies of RNA plus the enzymes reverse transcriptase, integrase and protease.
Envelope (of HIV): The outer layer, taken from the host cell plasma membrane, carrying viral glycoproteins.
What do the glycoproteins on HIV bind to?: CD4 receptors, proteins on the surface of helper T-cells.
Roles of reverse transcriptase, integrase and protease in HIV: Reverse transcriptase: makes DNA from the viral RNA template. Integrase: inserts the viral DNA into a host chromosome. Protease: cuts long viral proteins into functional lengths.
Replication cycle of HIV in order: Glycoproteins bind CD4 on a helper T-cell; RNA and enzymes enter; reverse transcriptase makes DNA; integrase inserts it into a host chromosome; it is transcribed and viral proteins made on host ribosomes, trimmed by protease; new particles are assembled and released.
Why does HIV infection leave a person vulnerable to other infections?: HIV destroys helper T-cells, which initiate the body's response to infections, so infections that are normally controlled become serious.
In drug-treated cells, viral DNA is found in the cytoplasm but not in a chromosome. Which enzyme is blocked, and with what effect?: Integrase. The DNA cannot be inserted into a host chromosome, so no new viral RNA is made from it.
Why do antibiotics not work against HIV?: Antibiotics act on bacterial structures and processes. A virus has no cell structure or metabolism of its own for them to act on.
Reverse transcription compared with transcription: Transcription makes RNA from a DNA template. Reverse transcription makes DNA from an RNA template.

3.2.5 The defensive functions of mammalian blood

Antigen: A molecule, usually a protein, that the immune system recognises as foreign and that triggers an immune response.
Antibody: A protein made by plasma cells that binds specifically to one antigen.
Phagocytosis in steps: Phagocyte is attracted to the pathogen and binds it; engulfs it into a phagosome; lysosomes fuse with the phagosome; hydrolytic enzymes digest the pathogen; antigens may be displayed on the phagocyte surface.
Cell-mediated and humoral immunity: Cell-mediated: the actions of T cells. Humoral: B cells, with antibodies in body fluids.
The B cell response in order: A macrophage presents the antigen; a T cell with a complementary receptor is activated; a B cell with a complementary surface antibody binds the antigen; it divides by mitosis (clonal expansion) into plasma cells, which secrete antibody, and memory cells.
Structure of an antibody: Two heavy and two light polypeptide chains joined by disulfide bridges. A variable region forms two identical antigen-binding sites; a constant region is the same within a class; a hinge gives flexibility.
Agglutination: Each antibody has two antigen-binding sites, so it can bind two bacteria, clumping them together; phagocytes then engulf the clumps.
Why is the secondary immune response faster and larger than the primary?: Memory cells made at the first exposure are already present. On re-exposure many recognise the antigen at once and divide rapidly into plasma cells, so more antibody is made sooner.
Active and passive immunity: Active: the body makes its own antibodies and memory cells (infection or vaccination); lasts years. Passive: ready-made antibodies are received (placenta, breast milk or injection); no memory cells; lasts weeks to months.
Herd immunity: Indirect protection of non-immune people, such as very young babies, when enough of the population is immune to stop the pathogen being transmitted.
How does antigen variability affect disease and vaccination?: If a pathogen's antigens change, existing memory cells no longer match, so people can be reinfected by a new strain and vaccines must be updated or are hard to make.
4 cases among 5000 vaccinated, 40 among 5000 on placebo. Calculate vaccine efficacy.: Attack rates: 0.08% and 0.8%. Efficacy = (0.8 − 0.08) ÷ 0.8 × 100 = 90%.

3.2.6 The circulation of blood and the structure of the mammalian heart

How is an artery wall adapted?: Thick, with elastic fibres that stretch and recoil to keep flow going between beats, collagen that stops the wall bursting, and smooth muscle that can narrow the lumen.
How are veins adapted to return blood to the heart?: Thin walls with little elastic tissue or muscle, a wide lumen (low resistance) and valves that stop backflow; skeletal muscles squeezing the veins push blood on.
How are capillaries adapted for exchange?: Walls one endothelial cell thick (short diffusion distance); very narrow, so red cells pass slowly and close to the wall; large total cross-section slows blood; gaps let fluid and small solutes out.
How is tissue fluid formed and returned to the blood?: At the arteriole end, high hydrostatic pressure forces water and small solutes out; cells and plasma proteins stay. At the venule end, hydrostatic pressure is lower and plasma proteins give a lower water potential, so water returns by osmosis. Excess drains into lymph.
Plasma, tissue fluid and lymph: Plasma: liquid part of blood inside vessels. Tissue fluid: plasma minus most of the protein, around the cells. Lymph: excess tissue fluid drained into lymph vessels.
Which vessels enter and leave each side of the heart?: Right atrium receives blood from the body via the vena cava; right ventricle pumps to the lungs via the pulmonary artery. Left atrium receives oxygenated blood via the pulmonary vein; left ventricle pumps to the body via the aorta.
Why does the left ventricle have the thickest wall?: It pumps blood at high pressure through the aorta to the whole body; the right ventricle pumps only to the nearby lungs.
What opens and closes the heart valves?: Pressure differences: a valve opens when the pressure behind it exceeds the pressure in front of it. Both sets are closed when ventricular pressure lies between atrial and arterial pressure.
Stroke volume and cardiac output: Stroke volume = end-diastolic volume − end-systolic volume (cm³ per beat). Cardiac output = heart rate × stroke volume (cm³ per minute).
Stroke volume 70 cm³, heart rate 72 beats per minute. What is the cardiac output?: 72 × 70 = 5040 cm³ per minute, which is 5.04 dm³ per minute.
What do the coronary arteries do?: They branch from the aorta and supply the cardiac muscle itself with oxygenated blood.

3.2.7 Heart disease may be associated with specific risk factors

Atheroma: Lipid-containing material within the artery wall.
Aneurysm: A weakened artery wall that bulges out and may burst.
Thrombosis: Damage to the artery lining starts clotting, and the clot (thrombus) can block the artery.
Myocardial infarction: A coronary artery is blocked, blood flow to cardiac muscle is interrupted, and the muscle beyond the blockage is deprived of oxygen and dies.
Chain from risk factors to a heart attack: High blood pressure, high blood cholesterol and smoking damage or load the artery wall, so atheroma forms; the lumen narrows and the wall weakens; thrombosis may follow; a thrombus in a coronary artery causes myocardial infarction.
How does smoking raise the risk of coronary heart disease?: Carbon monoxide reduces the oxygen the blood carries; nicotine raises heart rate and narrows vessels; smoking damages the artery lining.
How do diet and blood cholesterol affect the risk?: Saturated fat raises blood cholesterol, and a high concentration makes lipid deposits in artery walls more likely. Salt raises blood pressure.
How does high blood pressure raise the risk?: It damages the artery lining and stresses weak artery walls.
Exam trap: a risk factor compared with a cause: A risk factor is associated with a higher incidence of the disease; it is not proven to be the only cause. Name confounding variables (age, sex, activity, diet) and comment on sample size.

3.2.8 Mass transport systems in plants

Xylem: Tissue that carries water and mineral ions up the plant. The vessels are dead, with lignified walls.
Phloem: Tissue that carries organic substances, mainly sucrose, in sieve tubes with companion cells.
Apoplastic and symplastic pathways: Apoplastic: water moves through cell walls and the spaces between cells, without entering the cytoplasm. Symplastic: water moves through the cytoplasm of linked cells via plasmodesmata.
What happens to water at the endodermis?: The apoplastic route is blocked (by the waterproof suberin band in the walls), so water must enter the symplast before it passes into the xylem at the centre of the root.
Root pressure: Positive pressure pushing water up the xylem, produced when ions are actively moved into the xylem and water follows by osmosis. A small push only.
How is water pulled up the xylem?: Water evaporates from mesophyll cell walls and diffuses out through stomata (transpiration), putting the xylem under tension. Cohesion keeps the column unbroken; adhesion helps it cling to the walls.
Effect of light, temperature, humidity and air movement on transpiration: Brighter light: faster (stomata open). Higher temperature: faster (faster evaporation and diffusion). Higher humidity: slower (smaller vapour gradient). More air movement: faster (humid air swept away).
A potometer bubble moves 30 mm in 4.0 minutes in a tube of radius 0.50 mm. What is the rate of water uptake?: 7.5 mm per minute. Area = π × 0.50² = 0.785 mm². Uptake = 7.5 × 0.785 = 5.89 mm³ per minute. A potometer measures uptake, not loss.
Translocation, source and sink: Translocation: movement of organic substances in the phloem from sources to sinks. Source: releases sucrose into the phloem. Sink: uses or stores it.
Mass flow hypothesis: Sucrose is actively loaded into sieve tubes at the source; water enters by osmosis and hydrostatic pressure rises. At the sink sucrose is removed, water leaves and pressure falls. Sap flows down the pressure gradient.
Evidence for translocation in the phloem: Ringing: sugar accumulates above the ring. Radioactive tracers appear in the phloem. Sap flows out of an aphid stylet under pressure. Metabolic inhibitors reduce translocation, so loading needs energy.

3.2.9 The role of aphids in spreading plant viruses

Vector: A living carrier that moves a pathogen between hosts.
Stylet: The needle-like sucking mouthpart of an aphid, inserted into phloem vessels.
Why do plant viruses usually depend on vectors such as aphids?: Plants are immobile, so the virus needs a carrier to move between plants.
Why does phloem sap enter an aphid's gut without the aphid sucking hard?: Phloem sap is under high pressure, so once the stylet punctures a vessel the sap is forced into the aphid's gut.
How does an aphid spread a plant virus?: It inserts its stylets into the phloem of an infected plant and takes up virus in the sap. It moves to a healthy plant, inserts its stylets into that plant's phloem and passes the virus in.
Why do winged female aphids matter for the spread of plant viruses?: They migrate to new host plants and start colonies there, so the virus can reach plants and fields far from the source.
Symptoms of plant viral diseases and their effects: Yellowing of leaves (less chlorophyll, slower photosynthesis), leaf distortion (less light intercepted) and abnormal fruit or stunted growth, giving losses in crop yield and quality.
5 aphids double in number every 2 days. How many after 10 days?: 10 ÷ 2 = 5 doublings. 5 × 2⁵ = 5 × 32 = 160.

3.2.10 Cells divide by binary fission and mitosis

Phases of the cell cycle: G1: cell grows, more organelles and protein. S: DNA replicated. G2: rapid growth and protein synthesis. Mitosis: nucleus divides. G1, S and G2 together are interphase.
Prophase: Chromosomes condense and become visible; each is two chromatids joined at a centromere.
Metaphase: Chromosomes line up at the equator, with their centromeres attached to spindle fibres.
Anaphase: Centromeres divide; spindle fibres shorten and pull the chromatids to opposite poles.
Telophase: Chromosomes reach the poles, nuclear envelopes reform, and the cell divides.
A cell has 2n = 14. How many chromosomes in G1, after S phase, moving in anaphase, and in each daughter cell?: G1: 14. After S: 14 chromosomes (28 chromatids). Anaphase: 28 moving to the poles. Each daughter: 14.
Binary fission compared with mitosis: Binary fission: prokaryotes; circular DNA and plasmids copied; no spindle; plasmid number per daughter may vary. Mitosis: eukaryotes; linear chromosomes; spindle forms; two daughter cells with identical DNA.
Conjugation in bacteria: A copy of a plasmid passes from one bacterium to another, which may be a different species. This is horizontal gene transmission; vertical transmission is from parent to daughter cell.
Mitotic index: Number of cells in mitosis ÷ total number of cells counted (× 100 for a percentage). Divide by all cells, not only the dividing ones.
Root tip squash: why warm in hydrochloric acid, stain, and squash?: Acid softens the tissue so cells separate; a stain such as acetic orcein makes chromosomes visible; squashing gives one thin layer of cells to count.
15 bacteria divide every 40 minutes for 4 hours. How many cells?: 240 ÷ 40 = 6 divisions. 15 × 2⁶ = 15 × 64 = 960.

3.2.11 Mutation and cancer

Gene mutation: Any alteration to the order of bases in DNA. Mutations arise spontaneously during DNA replication.
Mutagen: A physical or chemical agent that increases the frequency of mutations.
Why may a base substitution not change the amino acid sequence?: The genetic code is degenerate: more than one triplet codes for the same amino acid, so the new triplet may code for the same one.
Why does a base deletion usually have a larger effect than a substitution?: It shifts the reading frame, so every codon after it is altered. A substitution changes only one codon (though it can create a stop codon).
Benign and malignant tumours: Benign: slower growth, often encapsulated, stays in place, cells similar to normal. Malignant: faster growth, invasive and irregular, spreads to form secondary tumours, cells often abnormal.
Proto-oncogenes and oncogenes: A proto-oncogene stimulates cell division. A mutation can turn it into an oncogene, which stimulates division too much.
Tumour suppressor genes in cancer: Normally they slow cell division. If a mutation inactivates one, the slowing is lost and the rate of division increases.
How do some anticancer drugs act on the cell cycle?: Some block DNA replication (acting in S phase); others prevent spindle formation (acting in mitosis), so chromatids cannot be separated.
Why do drugs that act on the cell cycle cause side effects?: Healthy cells that divide often, such as hair follicle and gut lining cells, are affected too.
Risk rises with alcohol intake: 3.1 cases per 100 000 for none, 16.5 for 5 or more units a day. What can you conclude?: 16.5 ÷ 3.1 = 5.3 times the risk, and a steady rise suggests a link. It shows correlation only: heavy drinkers may differ in other ways, such as smoking.