Term
|
Definition
|
|
Term
|
Definition
| group of similar, specialised, differentiated cells (e.g. capillary - just one type of cell) |
|
|
Term
|
Definition
| aggregation of tissues performing specific physiological roles |
|
|
Term
|
Definition
| organisation of organs performing life processes (7) e.g. reproductive, skeletal |
|
|
Term
|
Definition
| process of becoming adapted for specific function e.g. squamous epithelial cells |
|
|
Term
|
Definition
| movement of water molecules across membrane from high to low water potential |
|
|
Term
| water potential of pure water? |
|
Definition
|
|
Term
| adding solutes to pure water... |
|
Definition
| water potential more -ve water moves from high w.p. to low w.p. |
|
|
Term
|
Definition
| heart -> rest of body. Walls thick and muscular, lining (endothelium) folded to allow expansion to w/stand high pressure from systole. All carry oxygenated blood (not pulmonary) |
|
|
Term
|
Definition
| < artery. Network thru body. Direct blood to areas of demand by contracting/relaxing sphincter muscles (vasoconstriction/dilation) |
|
|
Term
|
Definition
| somatic --> heart. Wider lumen than equivalent artery, less elastic. Valves prevent backflow. Flow aided by contractions of skeletal muscle. All carry deoxygenated blood (not pulmonary veins) |
|
|
Term
| where is tissue fluid found? |
|
Definition
| bathes all cells in tissues |
|
|
Term
| composition of tissue fluid |
|
Definition
| substances that leave blood, e.g. oxygen, water (solute), nutrients. Waste from cells |
|
|
Term
|
Definition
| transports oxygen and nutrients to cells from blood, metabolic waste products from cell to blood |
|
|
Term
| how does tissue fluid leave blood in capillaries |
|
Definition
| 1) at arteriole end of capillary bed, pressure higher than in surrounding fluid so fluid is forced out (overcomes osmosis). 2) as it leaves, pressure decreases in capillaries increasing as nearer to vein end of capillary bed. 3) lower w.p. at vein end (+ lower pressure) means that some water can return to blood via osmosis, any excess drains back into blood via lymph system. Tissue fluid doesn't contain big proteins e.g. erythrocytes as these are too large to push btw walls. |
|
|
Term
| order of blood vessels heart --> heart |
|
Definition
| heart -> arteries -> arterioles -> capillaries -> veins -> heart |
|
|
Term
| how are capillaries adapted to function |
|
Definition
| walls: single layer, squamous epithelium, Narrow lumen = erythrocytes squashed flat = short diffusion path. Numerous/highly branched = large SA for diffusion. Narrow diameter = permeate tissues, near cells. Spaces between endothelial cells - w.b.c. can reach infection |
|
|
Term
| can capillaries serve every cell in body? |
|
Definition
| no - too many, tissue fluid needed |
|
|
Term
| 2 major adaptations of most gas exchange surfaces |
|
Definition
| high SA, thin - decrease diffusion path - maintains steep concentration gradient. Both increase RoDiff. |
|
|
Term
| 3 things that organisms need to exchange w/ environment |
|
Definition
| oxygen/nutrients, waste (e.g. carbon dioxide & urea), heat (regulate temperature) |
|
|
Term
|
Definition
| arteriole -> capillary (beds): smallest blood vessels. Efficient exchange of substances w/ cells. Always found near cells in exchange tissues (e.g. alveoli) - one cell thick so short diff. path. Large number = large SA for exchange. |
|
|
Term
| how does tissue fluid leave and return to blood? |
|
Definition
| 1. arterial end: high hydrostatic pressure forces tissue fluid (water, glucose, vitamins, minerals, amino acids, hormones) out - ULTRAFILTRATION. 2. after supplying substances to cells, tissue fluid must return to blood. At venule end, reduced hydrostatic pressure allows large proteins, too big to leave blood, to have osmotic effect: water (w/ waste) moves back into capillary. 3. remaining tissue fluid drains into lymphatic system where anti-backflow valves and contraction of skeletal muscles transports it back to the heart |
|
|
Term
|
Definition
| a range of chemicals that kill or inhibit growth of bacteria in a variety of ways |
|
|
Term
| how do (some) antibiotics work |
|
Definition
| 1. inhibit enzymes needed to make bonds in cell walls - prevents growth and weakens wall (permeable). 2. water moves into cell by osmosis 3. cell wall can't w/stand pressure and bursts - OSMOLYSIS |
|
|
Term
|
Definition
| 1. only used in life threatening situations: decrease antibiotic resistance vs. too much time off, lower standards of living, more suffering. 2. not for dementia sufferers: forget to take which increases resistance vs. their right to treatment. 3. not for terminally ill: increase resistance vs. decrease survival, lower life quality. |
|
|
Term
|
Definition
| cause range of infections: minor skin to life-threatening e.g. meningitis & septicaemia. Takes a long time to diagnose and prescribe right antibiotics during which time patient may die. Drug companies are therefore trying to develop alternative treatments. Reduce vectors e.g. doctors handwashing |
|
|
Term
| antibiotic resistance in mycobacterium tuberculosis |
|
Definition
| vaccine lowered infection/death rate. NS favoured multi-drug resistant strains in population so evolved resistance. Now a 6 month drug regime is required, however the bacterium is still evolving so drug co.s need to stay ahead of the curve. |
|
|
Term
| what are mutations and how do they give rise to new characteristics |
|
Definition
| 1 or more bases added, deleted, replaced during replication. --> different primary protein structure (amino acid sequence). --> different protein/enzyme --> disruption of metabolic pathways leading to production of other substances, including proteins, e.g. those responsible for characteristics. |
|
|
Term
| why is antibiotic resistance on the rise? |
|
Definition
| doctors under pressure to prescribe for minor ailments. Used to treat viral diseases & secondary infections. Courses not completed. Patients stockpile for use later. Over-use in intensive farming |
|
|
Term
| how is antibiotic susceptibility in bacteria determined? |
|
Definition
| suitable urine/blood/stool etc made into suspension of bacteria, placed on nutrient agar and incubated. Antibiotic disks are placed on agar and relative zone of inhibition compared. Paper disk used as control. |
|
|
Term
| how can mutations in bacterial DNA lead to antibiotic resistance? |
|
Definition
| Mutations: change in DNA base sequence -> proteins -> characteristics i.e. antibiotic resistance. E.g. MRSA: methicillin can't inhibit enzyme that builds cells walls due to altered enzyme structure. Osmolysis can't occur |
|
|
Term
| how is antibiotic resistance passed on? |
|
Definition
| vertical - bacteria reproduce asexually (nt mitosis) - e/ daughter exact copy of parent (incl genes & antibiotic resistance in plasmid loop). Horizontal - 2 bacteria join via conjugation tube; copy of part of plasmid loop passed across |
|
|
Term
| why is MRSA especially prevalent and dangerous in hospitals? |
|
Definition
| patients older, sicker, weaker than general population - more vulnerable to infection. They are in close proximity, staff act as vectors. More antibiotics are used so more mutant strains. |
|
|
Term
|
Definition
| abnormality of organism that affects performance of vital functions and usually gives diagnostic signs |
|
|
Term
|
Definition
| a few isolated individuals in localised area contract disease |
|
|
Term
|
Definition
| outbreak in large number of population in several communities (but not across significant barriers) |
|
|
Term
|
Definition
| epidemic across continents |
|
|
Term
| 7 types of disease and their risk factors |
|
Definition
| Allergic - hyposensitivity to antigens. Deficiency - not enough nutrients (e.g. scurvy). Degenerative - old age. Genetic - gene mutations. Infectious - living organisms, communicable. Lifestyle - smoking, diet etc. Mental - Alzheimer's etc. |
|
|
Term
| 3 ways pathogens penetrate organism's interface w/ environment and how organism resists. |
|
Definition
| Gas exchange system - invade cells in alveoli - trapped in droplets of mucus in lung epithelium - moved by cilia to stomach where destroyed by HCl. Skin - pathogens enter blood via damaged skin - clotting helps to prevent. Digestive system - survive HCl and infect intestinal epithelium |
|
|
Term
|
Definition
| a measure of the probability that damage to health will occur as a result of a given hazard, i.e. something that increases the risk of contracting a specific disease |
|
|
Term
| what are the risk factors for CHD |
|
Definition
| (lifestyle) 1. poor diet: high in saturated fat and salt. 2. smoking, lack of exercise, alcohol --> hypertension --> heart & vascular system damage |
|
|
Term
|
Definition
|
|
Term
|
Definition
| bacteria, fungi, virus or parasite (micro/macro e.g. tapeworm) |
|
|
Term
|
Definition
| chicken pox, small pox, polio, flu, measles, colds (most), AIDs |
|
|
Term
|
Definition
| nearly all on body surface e.g. ringworm, athlete's foot, thrush (candida) |
|
|
Term
| e.g.s of bacterial diseases |
|
Definition
| cholera, TB, food poisoning (salmonella, E. Coli), MRSA |
|
|
Term
| in what ways do pathogens cause disease |
|
Definition
| 1: production of toxins e.g. bacteria that causes tetanus produces toxins that block function of certain nerve cells which causes muscle spasms. 2: Cell damage e.g. physical damage, rupturing to release nutrients/proteins etc, digesting nutrients for own use (starvation -> death), replication inside cells --> lysis e.g. some viruses |
|
|
Term
|
Definition
| uncontrolled cell division |
|
|
Term
|
Definition
| 1. smoking - mouth, throat, lung 2. high UV exposure (i.e. sunlight) - skin 3. alcohol - many e.g. liver |
|
|
Term
| most effective way of reducing CHD & cancer risk factors |
|
Definition
|
|
Term
| difference between correlation and causal relationship |
|
Definition
| correlation - observed relationship between variables, not definitive. Causal relationship - overwhelming evidence from carefully designed experiments where variables can be controlled to prove a hypotheses about an observation e.g. 'smoking causes cancer' |
|
|
Term
|
Definition
| study of spread of disease & factors that influence its spread |
|
|
Term
|
Definition
| pathogens spend part of life-cycle in/on another species - e.g occasionally affect people |
|
|
Term
|
Definition
| microbes that normally co-exist w/ host (e.g. skin, gut) enter through damaged/immunocompromised barrier and cause disease |
|
|
Term
|
Definition
| enzymes are proteins which catalyse metabolic reactions e.g. digestion & respiration (growth & development). They have an active site with a specific shape complementary to their substrate. Their complex tertiary structure means they are highly specific |
|
|
Term
| how do enzymes speed up reactions |
|
Definition
| lower activation energy (amt energy, often heat, needed for rxn to start) so rxn can occur at a lower temperature |
|
|
Term
|
Definition
| 3 main pairs around mouth. Secrete saliva: (mucus, mineral salts & amylase: starch --> maltose) lubricates to aid swallowing |
|
|
Term
|
Definition
| links mouth to stomach. Undergoes peristalsis and secretes mucus to lubricate bolus and trap pathogens |
|
|
Term
|
Definition
| folded to increase SA, Sphincters (pyloric & gastrooesophageal) to control entrance & exit. Secretes gastric juice (HCl, pepsin [protease], mucus) + peristalsis (churning) breaks down food = chyme (low pH) |
|
|
Term
|
Definition
| first section of small intestine |
|
|
Term
|
Definition
| secretes pancreatic juice (amylase, trypsin, chymotrypsin) & sodium hydrogen carbonate which neutralises HCl |
|
|
Term
|
Definition
| main section of small intestine. Undergoes peristalsis. High SA as folded into villi. Bile (detergent) & pancreatic juice further breaks down neutralised chyme e.g. into glucose, amino acids & fatty acids, which are then absorbed through villi (by diffusion, facilitated diffusion & active transport). |
|
|
Term
|
Definition
| Large intestine. Absorbs water, salt & minerals. High SA. Contains hugh diversity of anaerobic bacteria |
|
|
Term
|
Definition
| Stores faeces prior to defacation |
|
|
Term
|
Definition
| Bieuret test: add few drops of NaOH (so alkaline). Add Copper(II) sulfate solution. Purple = present, Blue = absent. |
|
|
Term
| why do polymers in food need to be broken down |
|
Definition
| to be absorbed and assimilated into new products |
|
|
Term
| how are polymers in food broken down |
|
Definition
| insoluble in water so hydrolysed by digestive enzymes |
|
|
Term
| what bond is hydrolysed in carbohydrate digestion |
|
Definition
|
|
Term
| what bond is hydrolysed in protein digestion |
|
Definition
|
|
Term
| difference between different amino acids |
|
Definition
| different R functional groups |
|
|
Term
| how are amino acids joined together into polypeptides |
|
Definition
| condensation rxn - removal of water molecule btw hydroxyl of carboxylic acid of one and nitrogen of amine group of other (peptide bond) |
|
|
Term
| describe RoR vs [s] graph: unlimited enzyme |
|
Definition
| amount of substrate limits RoR, rate increases proportionally with [s] because always unoccupied active sites |
|
|
Term
| describe RoR vs [s] graph: fixed amount of enzyme |
|
Definition
| up to point of inflection, substrate concentration is limiting factor because there are unoccupied active sites. Beyond point of inflection, RoR is constant w/ increasing [s] because active sites are saturated. |
|
|
Term
|
Definition
| catalyse carbohydrate hydrolysis |
|
|
Term
|
Definition
| catalyse protein hydrolysis |
|
|
Term
|
Definition
| catalyse lipid hydrolysis |
|
|
Term
| what kinds of food are rich in proteins |
|
Definition
|
|
Term
| what kinds of food are rich in carbohydrates |
|
Definition
|
|
Term
|
Definition
| composed of amylose and amylopectin which are both long chains of alpha glucose with glycosidic bonds between monomers, these are broken down in condensation reactions |
|
|
Term
| 1st and 2nd stage of starch digestion |
|
Definition
| 1st: starch --> maltose (salivery/pancreatic amylase). 2nd maltose --> alpha glucose monomers (intestinal epithelium maltase) |
|
|
Term
|
Definition
| add iodine dissolved in potassium iodide solution. +ve: browny orange to blue-black |
|
|
Term
|
Definition
| hexose, 6C (O atom in hexagon, 6th carbon on branch) |
|
|
Term
| what type of sugar is alpha glucose |
|
Definition
| hexose, 6C (O atom in hexagon, 6th carbon on branch) |
|
|
Term
| how does alpha glucose form di/polysaccharides |
|
Definition
| condensation reaction produces glycosidic bonds between 2 or more monomers |
|
|
Term
| salivary glands: enzyme(s), class, hydrolyses... |
|
Definition
| amylase (carbohydrase: starch --> maltose) |
|
|
Term
| stomach: enzyme(s), class, hydrolyses... |
|
Definition
| pepsin (protease: proteins --> peptides) |
|
|
Term
| pancreas: enzyme(s), class, hydrolyses... |
|
Definition
| amylase (carbohydrase: starch --> maltose), trypsin (protease: protein --> peptides), chymotrypsin (protease: protein --> peptides), carboxypeptidase (protease: peptides --> amino acids), lipase (lipase: lipids --> fatty acids + glycerol) |
|
|
Term
| ileum: enzyme(s), class, hydrolyses... |
|
Definition
| maltase (carbohydrase: maltose --> glucose), sucrase (carbohydrase: sucrose --> fructose + glucose), lactase (carbohydrase: lactose --> glucose + galactose), peptidase (protease: peptides --> amino acids) |
|
|
Term
|
Definition
| break down large molecules into smaller soluble molecules to be absorbed and assimilated |
|
|
Term
| monomers of carbohydrates |
|
Definition
|
|
Term
| elements in monosaccharides |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
| gene for lactase switched off (evolved away from cow's milk) so lactose can't be digested and absorbed. Lactose solute lowers water potential of lumen so water moves into lumen by osmosis. This: dilutes digestive enzymes so digestion is slower; dilutes digestive products so absorption is slower (nutrition less effective) - this is more acute in colon which is the site of water absorption --> diarrhea; lactose also feed anaerobic bacteria --> flatulence & stomach cramps. The patient should only drink lactose-free milk (lactose beads) or alternatives to milk |
|
|
Term
| non-competitive inhibition |
|
Definition
| non-competitive inhibitor binds elsewhere than active site. It changes tertiary protein structure and therefore shape of active site so substrate won't fit, so an increase of substrate concentration does not effect enzyme activity |
|
|
Term
| How does tertiary structure relate enzyme properties |
|
Definition
| Shape of active site is determined by tertiary structure which in turn is determined by primary protein structure. This means enzymes are very specific; only one shape of substrate is complementary to a.s. so catalyses 1 type of reaction. Tertiary structure can be altered by changes in temperature and pH, or primary structure (sequence of amino acids) changed by gene mutation --> no rxn. |
|
|
Term
| how do enzymes catalyse catabolic rxns |
|
Definition
| cata- - break down - substrate in active site puts strain on bonds so they break more easily |
|
|
Term
| how do enzymes catalyse anabolic rxns |
|
Definition
| substrate molecules held close together in active site, overcoming any repulsion so bond more easily |
|
|
Term
| what's the name for the substrate and enzyme when bound |
|
Definition
| ESC - enzyme-substrate complex |
|
|
Term
| what are reducing sugars? e.g.s |
|
Definition
| donate electrons. All monosaccharides, lactose and maltose |
|
|
Term
|
Definition
| add benedict's reagent (blue). Heat. positive: brick red |
|
|
Term
|
Definition
| boil w/ dil. HCl to break glycosidic bonds -> monosaccharides. Neutralise w/ NaOH. Perform Benedict's test |
|
|
Term
| lock and key model of enzyme action, evidence against, better model? |
|
Definition
| substrate complementary shape to a.s.. It's been observed that substrate and enzyme change shape when substrate binds. The Induced Fit Model explains how enzyme activity can be affected by variety of factors: the change of shape puts strain on bonds and lowers activation energy |
|
|
Term
|
Definition
| similar molecular shape as substrate so competes for and blocks a.s. - degree of inhibition depends on relative concentrations of inhibitor + substrate. (Reversible - substrate has higher affinity for a.s. than inhibitor) |
|
|
Term
|
Definition
| enzymes (often spherical - tight folding - often metabolic, digestive, synthetic roles), antibodies (involved in immune response. 2 light (short) + 2 heavy (long) polypeptide chains, variable regions - amino acid sequence varies greatly), transport proteins (in cell membranes. Hydrophobic + hydrophilic amino acids so folds into channel to transport molecules and ions), structural proteins (strong, long polypeptide chains w/ parallel + cross links e.g. keratin (hair & nails) collagen (connective tissues) |
|
|
Term
| how does pH influence enzyme activity |
|
Definition
| H (low pH) & OH (high pH) ions affect ionic and H bonds --> deactivation (change shape) --> denaturation. (in humans, optimum pH is around 7 except e.g. pepsin in stomach around pH 2) |
|
|
Term
| 3 factors which affect rate of enzyme catalysed reactions |
|
Definition
| 1) ratio + absolute concentration of enzyme/substrate 2) environmental: pH & temperature 3) inhibitors |
|
|
Term
| examples of enzyme inhibitors |
|
Definition
| some poisons e.g. cyanide (inhibits final enzyme of electron transport chain in mitochondria), some drugs e.g viagra, aspirin, penicillin |
|
|
Term
| how does temperature influence enzyme activity |
|
Definition
| higher temperatures - molecules vibrate more. Collision theory: higher k.e. --> more forceful + frequent collisions --> higher activity. Too high temperatures will break bonds in tertiary structure (H 1st) leading to deactivation and denaturation --> change in shape |
|
|
Term
|
Definition
| temperature below optimum for digestive enzymes |
|
|
Term
| how does enzyme increase rate of biological reactions? |
|
Definition
| lower activation energy (amt energy, often heat, needed for rxn to start) so rxn can occur at a lower temperature |
|
|
Term
| primary protein structure |
|
Definition
| specific sequence of amino acids |
|
|
Term
| secondary protein structure |
|
Definition
| polypeptide coils - amino acids form H-bonds w/ e/other - alpha helix or beta pleated sheet |
|
|
Term
| tertiary protein structure |
|
Definition
| further folding of secondary structure, disulfide bridges and ionic bonds form btw R groups, H-bonds. Single polypeptide forms a final, specific 3D structure |
|
|
Term
| quaternary protein structure |
|
Definition
| >1 polypeptide + prosthetic groups (e.g. haemoglobin, immunoglobulin, many enzymes, insulin, collagen) |
|
|
Term
| what does the specific shape of a protein determine |
|
Definition
|
|