Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Bio topic 6
| Question | Answer |
|---|---|
| Methods of determining time of death | Extent of decomposition Core body temperature Forensic entomology Rigor mortis |
| Extent of decomposition | Autolysis first (body's own digestive enzymes break down body cells) - putrefaction causes discolouration of the body between 36-72hrs (greenish at abdomen, starts darkening and spreading) - blisters and bloating due to gases from bacteria in 1 week |
| Core body temperature | Core body temp 36.2-37.6 and starts dropping as soon as death occurs. Cooling follows a sigmoid curve from core to ambient temp. Useful within first 24hrs. Largely affected by environmental conditions e.g clothing, body size, humidity |
| Forensic entomology | Pioneer species (e.g bluebottle) colonise the body and lay eggs. Size of maggots can be measured to figure out the correct instar stage and backdate how long ago the eggs were laid. Over time More organisms colonise, pioneers tend to remain. |
| Rigor mortis process | 1. Muscles starved of O2 after death 2. Anaerobic respiration occurs building up lactic acid 3. pH falls, inhibiting enzymes and anaerobic respiration 4. ATP not produced, actin and myosin fixed 5. Proteins can't move over each other, muscles fixed |
| Rigor mortis for time of death | Warm/Flaccid - <3hrs Warm/Stiff - 3-8hrs Cold/Stiff - 8-36hrs Cold/Flaccid - >36hrs (flaccid as muscle tissue broken down) |
| Decomposers | Insects, bacteria, fungi - help release CO2 back to atmosphere |
| DNA profiling | STRs in DNA amplified with PCR, separated by gel electrophoresis, visualised with southern blotting Each band is a different STR, the number of STRs and whether they are on the same loci in homologous chromosomes are unique to a person - identification |
| PCR (Polymerase chain reaction) | Uses a sample of DNA (e.g hair) with DNA primers and nucleotides 1. Denaturation - separates strands 95C 2. Annealing - primers attach to start of STR sequence 55C 3. Extending - taq polymerase joins nucleotides replicating the DNA 70C Cycle repeated |
| Gel electrophoresis | STRs are micropipetted into wells of agarose gel which is in a buffer solution. Electricity passed through, negatively charged DNA fragments move to the anode. Larger, heavier fragments move slower so are closer to well - more repeats = heavier fragment |
| Southern blotting | DNA transferred to nylon sheet drawn up with buffer solution - also denatures into single strands. Mixed with DNA probes which bind to complementary fragments. If radioactive marker- X-ray, if fluorescent - UV used to visualise |
| Bacteria structure | Always: Peptidoglycan cell wall, cell membrane, main circular DNA, ribosomes (smaller than eukaryotic cells), mesosome Sometimes: Plasmids, flagellum, capsule, pili |
| Virus structure | Protein coats surrounding nucleic acid (DNA/RNA). Sometimes capsid made of protein units around nucleic acid. Sometimes a surrounding layer of glycoprotein stolen from host cell. HIV has 2 RNA, reverse transcriptase and integrase in the capsid. |
| TB infection | Typically enters through lungs - macrophages engulf TB and build up forming a granuloma. Once engulfed, TB can evade the killing mechanisms and lie dormant. If the immune system weakens, TB can become active destroying lung tissue killing the person |
| HIV infection | 1.gp120 binds to CD4, membranes fuse, contents released 2.Reverse transcriptase turns 2RNA into 1DNA 3.Integrase inserts HIV DNA in host DNA 4.HIV proteins+ envelope proteins translated 5.Proteins assemble new virus, buds out T helper cell killing it |
| AIDS | Acute phase - Initial infection , infection fought but not eliminated Chronic phase - virus remains dormant, may reactivate other dormant diseases e.g TB, shingles Disease phase - rapid decline in T helper cells leads to fatal opportunistic infections |
| Non-specific immune response | Inflammation, Lysozymes, Interferon, Phagocytosis |
| Inflammation | Damaged white blood and mast cells release histamine causing arterioles to dilate increasing blood flow. Capillaries become more permeable causing plasma, white cells and antibodies to leak. Infecting microbes can now be attacked by intact white cells |
| Lysozymes | Enzyme found in tears, saliva, and nasal secretions that kill bacteria by breaking down their cell walls |
| Interferon | A protein produced by infected cells which inhibits microbial protein synthesis preventing multiplication. Provides defence against viruses primarily. |
| Phagocytosis | Involve neutrophils (70% of wbcs) and monocytes which become macrophages (4% of wbcs) Membrane of cell extends around the bacteria and encloses it in a vacuole. Lysosomes fuse with the vacuole releasing enzymes that destroy the bacteria |
| Antigen presenting cell (APC) | In phagocytosis, the antigens can become attached to proteins in the cell and be added to the cell surface membrane. B cells become APCs when binding to bacteria antigen Cells can become APCs when infected |
| B lymphocytes | Produced in the bone marrow B effector - differentiate into plasma cells which release antibodies, relatively short lived (a few days) B memory - remains in blood for months or years allowing faster response if infected by same antigen again |
| T lymphocytes | Produced in bone marrow, matures in thymus gland T helper - stimulate B cells and T killer cells to divide, enhanced phagocytosis T killer - destroys cells with foreign antigens T memory - remains in blood allowing faster response if infected again |
| Activation of T helper cells | 1. Macrophage engulfs bacteria and becomes APC 2. APC binds to complementary CD4 receptors on T helper 3. T helper is activated and divides into active T helper cells and memory T helper cells |
| Clonal selection | 1. Antigens bind to B cell making it an APC 2. Active T helper with complementary receptor binds to APC, cytokines produced stimulating B cell 3. B cell divides to B memory + B effector 4. B effector differentiates to plasma cells - secretes antibodies |
| Role of T killer cells | 1. Cell gets infected and becomes an APC 2. T killer w/ complementary receptor binds to it 3. Cytokines stimulate division & differentiation into active T killer + T killer memory 4. Active T killer binds to infected cell, chemicals cause pores, lysis |
| Antibodies | 1. Secreted by plasma cells 2. Binds to/neutralises antigens and labels/opsonise them 3. Antibodies then bind to antibody receptor on macrophage 4. Macrophage engulfs antibody+bacteria in a vacuole releasing lysosomes killing them |
| Agglutination | Antibodies have 2 binding sites and can aggregate multiple pathogens making it easier for macrophages/neutrophils to ingest |
| Post transcription modifications | Before translation, mRNA can be edited by non coding introns being removed and the remaining exons being spliced together in different arrangements. Thus one gene can give rise to more than one protein |
| Major routes of entry for pathogens | Respiratory tract, breaks in the skin, digestive tract, genital tract (STDs), eyes, nose/mouth |
| Preventing pathogen entry (skin + mucous membranes) | Skin - Keratin is hard and cant be gotten through easily, blood clots block entry through wounds, skin flora is bacteria which colonises the skin and outcompetes pathogens Mucous membranes - mucus in airways and gut trap pathogens, cilia move them out |
| Preventing pathogen entry (Stomach acid + gut flora) | Stomach acid - low pH kills most pathogens Gut flora - like skin the intestines are colonised by bacteria adapted to those conditions and so they outcompete pathogens preventing their colonisation |
| Immunity | Natural - antibodies come from a natural source e.g placenta Artificial - antibodies come from a human made source e.g vaccines Active - body is producing its own antibodies Passive - body is being given antibodies from an outside source |
| 'Evolutionary race' | Bacteria are evolving to evade our immune systems, our immune systems are evolving to avoid pathogens Bacteria have a slight edge due to rapid reproduction (vertical) and conjugation - passing plasmids between bacteria through pili (horizontal) |
| Antibiotics | Bactericidal - kills the bacteria e.g through lysis Bacteriostatic - prevents bacterial reproduction letting the immune system kill the bacteria e.g inhibiting protein synthesis |
| CORE PRACTICAL 15: Investigate the effect of different antibiotics on bacteria | Aseptic technique - using an autoclave to sterilise forceps, wiping surfaces with detergent, using the petri dish in presence of a Bunsen burner to kill bacteria in the air The more effective bacteria has the larger area of inhibition |
| Hospital acquired infections/Healthcare associated infections (HCAIs) | Bacteria evolving to be antibiotic resistant - mainly due to misuse of antibiotics e.g over prescription, not finishing a course HCAIs also refer to infections caught in hospitals due to poor infection control - led to better practices e.g hand washing |
Created by:
silver54331