| How does the immune system distinguish between body cells and foreign cells? (2) | eliminates foreign material
all nucleated cells have distinctive surface molecules = self |
| What are the self markers on cells called? what do they do? (3) | major histocompatibility molecules (MHC class 1)
identity tags for the bodies
immune system does not react to the cells |
| What is an antigen? | foreign to the body so it triggers immune system |
| How are antigens recognized? (3) | lymphocytes
bind
detect the shape of an exposed portion of the antigen called epitope |
| How do lymphocytes destroy antigens? | lymphocytes produce antibodies (Adaptive immunity) which binds to epitope through complementary paratopes |
| What is the exposed portion of an antigen called? | epitope |
| How do antibodies attach to antigens? (method name) | complementary paratopes |
| What are features of an antigen? (2) | surface markers in blood and tissue - bacterial, fungal, viral and parasitic
self markers of diff organisms |
| What are the different types of surface markers found? (4) | bacterial, fungal, viral and parasitic |
| Why doe RBCs not have self markers? how are they recognized? (3) | not nucleated = no self markers
so RBCs can be transferred bw individuals
but they have antigenic markers (limits transfusion ability) = ABO |
| What are the antigenic markers in RBCs called? (2) | ABO system
surface glycoproteins |
| What are the differences in the ABO system? (2) | RBC can have A or B surface glycoproteins independently or together
or have neither (O) |
| Why do blood transfusions sometimes not work? | because people produce antibodies against foreign antibodies (diff blood type would have diff antigenic markers) |
| What blood groups are each of them compatible with? (4) | AB = all
A = A or O (B isoantigen is foreign)
B = B or O
O = only O |
| What causes the negative or positive blood groups? | Rhesus factor glycoprotein is either present or absent = + or - |
| What happens with incompatible blood transfusion? (3) | surface antigens + opposing antibodies
= agglutination (clumping)
= hemolysis (RBCs destroyed so O2 released into surroundings) |
| What is a pathogen? (3) | agent that causes disease
recognized by its antigens
eg: bacteria, protist, fungi, parasite |
| What is a disease? | affects normal functioning (can't maintain hemostasis) |
| What is an illness? | deteriorates normal health |
| Why do some pathogens only affect humans? | usually species specific in pathogenesis
EG: polio, syphilis, measles |
| What are zoonotic diseases? (2) | from animals to humans
eg: rabies (dogs) , influenza (birds), bubonic plague (rats) |
| What are different ways in which disease can be transmitted? (Disgusted Cats Are Vicious) | Direct contact - physical touch / exchanging body fluids
Contamination - ingesting pathogens in food
Airborne - coughing or sneezing
Vectors - intermediary organisms that transfer pathogens w/o developing symptoms themselves |
| What is clonal selection? | process of matching antigens w/ antigen receptors on B and T lymphocytes |
| What are the steps in fighting a pathogen? (6) | 1) non specific - macrophage engulf pathogens and breaks them down
2) dendritic cells have the antigen fragments and present them to specific T helper lympho which activates it
3) cytokines released
4) cytokines activate specific B cell to produce antibodies which divides and forms clones
5) clones become short lived plasma cells that produce a large quantity of an antibody
6) small group of clones become long living memory cells for immunity |
| Why are several lymphocytes activated at the same time? what is this called? (3) | pathogens can have multiple antigenic fragments
so different lymphocytes activated for different antibodies
= polyclonal activation |
| What are the different methods of antibodies destroying pathogens? PANIC | Precipitation = soluble pathogens -> insoluble = solid
Agglutination = clumped for easy removal
Neutralization = block pathogenic regions (exotoxins = proteins released by bacteria to change cell structure)
Inflammation = inflammatory response within body (histamine released)
= these 4 help w/ phagocytosis
Complement activation = complement proteins destroy membranes (cell lysis) |
| What are macrophages? | phagocytic leukocytes |
| What is it called when pathogens are identified? (2) | opsonisation - when opsonins (Antibodies) bind to bacterial cell which makes it easier for phagocytes to engulf it |
| What are memory cells? what do they do? (3) | made from plasma cells to prevent delay after exposure to prevent symptoms developing
long living
reacts quickly if infected w the same pathogen |
| What is an allergen? what is the response like?(2) | environmental substance that triggers an immune response even though it isnt harmful
response is specific to exposure region (throat) = allergic reaction |
| What is a severe allergic reaction called? | anaphylaxis |
| What are the stages of an allergic reaction? | first exposure (sensitization):
1) allergen (cat hair) enters blood
2) B cells = plasma cells = antibodies (IgE)
3) antibodies attach to mast cell (has histamine inside)
second exposure (allergic reaction):
1) allergen binds to antibodies on mast cell
2) histamine released
3) allergic reaction from inflammation from histamine |
| What do mast cells do? | allergy WBC cells that cause inflammation w histamine |
| What are IgE antibodies? | immunoglobulin antibodies attach to mast cells to release histamine to cause inflammation if an allergen is detected |
| What are histamines? | chemicals released by WBCs when the immune system is defending against an allergen
causes inflammation |
| How does an inflammatory response help defend against allergens? (5) | improves leukocytes movement by causing vasodilation + capillary permeability
capillary widening = increases blood flow
increased permeability = fluid release into tissues
attraction of leukocytes
systemic response = fever and increasing of leukocytes |
| What does vasodilation cause? consequence? (3) | widens blood vessels = better blood flow
redness because it moves blood closer to skin
heat |
| what does capillary permeability do? consequence? (3) | how much leukocytes leave the bloodstream
leads to swelling (more fluid leaks)
pain (nerve compression) |
| What are the symptoms of inflammation? (5) | heat
redness
swelling
tenderness
pain |
| What are vaccines? (3) | contain antigen determinants trigger immunity but doesn't cause the disease
produces memory cells
can be conjugated w an adjuvant (boosts immune response) |
| what is an adjuvant? | a substance that enhances the immune systems response to an antigen |
| What happens when injected with a vaccine? (3) | a primary immune response = memory cells made
Actual pathogen = memory cells cause better secondary response
symptoms dont develop |
| How is the immunity length from a vaccination determined? (3) | depends on how long the memory cells survive
may not survive a lifetime
may need a booster shot for immunity |
| what is the weakened form of a pathogen called? | attenuated form |
| How does herd immunity work with vaccines? | when individuals who aren't immune to the pathogen are protected from exposure by large amounts of immune people |
| what is an epidemic? | increasing infection in a region |
| what is a pandemic? | epidemic spread across a large geographical area |
| What is small pox? how was it so easily treated? (6) | first disease eradicated by vaccinations in 1967 by WHO
easily identified bec of overt symptoms = limit transmission
only transmitted through direct contact
short lived infection and no mutations
global cooperation
long term immunity |
| reasons for changes in pandemic trends? | populations increase = increase risk of outbreaks
improvement of health services = decrease disease rates
diff regions have diff exposure levels |
| What are monoclonal antibodies? | articifical antibodies from a single B cell clone (identical and specific antibodies) |
| What is the process of creating monoclonal antibodies? (3) | animal (mouse) injected w antigen = antigen specific plasma cells
removed and fused w tumor cells to form hybridoma cell = endless divisions
can make a large amount of antibody |
| benefits of monoclonal antibodies | identical
specific antibodies produced
produced in a large quantity
endless divisions
relatively easy and cheap |
| What are uses of monoclonal antibodies? | rabies
detecting pregnancy |
| How is monoclonal antibodies used for diseases (2) | immune protection
targets cancer cells that the body's own immune cells can fail to recognise as bad |
| How is monoclonal antibodies used to detect pregnancy? | hCG = human chorionic gonadotrophin in urine = made during fetal development
ELISA = enzyme linked immunosorbent assay = Identifies substance by color change |
| What is ELISA? | enzyme linked immunosorbent assay = pregnancy test |
| What is the process of ELISA? (5) | Monoclonal antibodies for hCG is conjugated to enzyme that changes dye color
2nd set of monoclonal antibodies specific to hCG immobilised to dye substrate
if hCG present in urine = reacts with both sets of monoclonal antibody
changes color
3rd set of monoclonal antivodies bind to unattached enzyme linked antibodies |
| What are examples of the first line of defense? (4) | skin and mucous membranes
lactic acid and fatty acids on the skin lowers pH (5,6)
mucus washes away pathogens
lysozymes in tears can cause cell lysis
cilia in the trachea can help remove pathogens |
| What is clotting? | how broken blood vessels are repaired when damaged = prevents blood loss and pathogenic access |
| What are the steps in the coagulation cascade for blood clotting? (5) | 1) damaged cells and platelets = clotting factors
2) clotting factors = platelets become sticky = plug and reduced blood flow to damaged region
prothrombin = thrombin (activated)
3) thrombin = converts fibrinogen to fibrin (insoluble)
4) fibrin forms mesh around platelet plug = clot
5) when repaired = plasmin dissolves clot |
| What is coronary thrombosis? | when a cloth forms in a coronary artery (to heart) = acute myocardial infraction (heart attack) |
| what is atherosclerosis? | deposition of cholesterol = damages blood vessels - blood clots form |
| What are the steps in forming blood clots in coronary arteries? (6) | 1) atheromas (fatty) = reduces artery lumen diameter
2) less blood flow = +P = damages artery wall
3) wall repaired w fibrous tissue = less elasticity
4)atherosclerotic plaque forms
5) if plaque ruptures = blood clotting = thrombus
6) if thrombus moves = embolus = blocks small arterioles |
| What is the second line of defence? key features? (3) | non specific (doesnt differentiate) and non adaptive (responds in the same way)
phagocytes |
| What is the process of phagocytosis? (5) | phagocytic leukocytes enter tissue in response to an infection (extravasation)
damaged tissues release histamaine = draws WBC to infection (chemotaxis)
pseudopodia surround pathogen and fuse to form vesicle
fuses w lysosome = phagolysosome = digested
antigens are present on phagocyte which is destroyed w antibodies |
| what is the third line of defence? | lymphocytes( B and T cells) produce antibodies to have a specific and adaptive response against antigens |
| What are B cells? | produce antibodies that recognise a specific antigen |
| What are T cells? | release cytokines to activate specific B lymphocytes |
| What is an antigen? | body recognises it as foreign and causes an immune reponse |
| What is an antibody? (4) | protein made by B and plasma cells that are specific to an antigen
4 pp chains joined w disuplhide bonds
ends = variable regions
recognition site for immune system (opsonisation) |
| What are antibiotics? (5) | kill bacteria by targeting pro metabolism
enzymes, 70s ribosomes, cell wall
doesn't target infected host bec doesn't affect euk cells
doesn't affect viruses bec they don't have a metabolism
narrow or broad spectrum |
| How are viruses treated? (2) | antiviral agents
target viral enzymes (reverse transcriptase /caspid) |
| How do bacteria gain antibiotic resistance? (3) | encode traits that degrade antibiotic
block entry
increase removal |
| Why does antibiotic resistance increase quickly? (2) | bacteria reproduce quickly
bacterial conjugation (horizontal gene transfer) |
| Why is resistant bacteria strains increasing among humans? (4) | antibiotics being over prescribed (broad spectrum) / misused
freely available w/o prescription
used in livestock feed
resistant bacteria is common in hospitals (Nosocomial) |
| Example of antibiotic resistant strain? | Golden Staph (MRSA - Methicillin Resistant Staphylococcus aureus |
| What is penicillin? evidence? (2) | antibiotic found by Fleming
ring of inhibited bacterial growth on plate |
| How was the medical applications of penicillin proved? (4) | Florey and Chain tested penicillin on infected mice
8 were injected w hemolytic streptococci
4 with penicillin
untreated mice died while those treated survived = potential antibiotic |
| What is HIV? and AIDS? (2) | Human immunodeficiency Virus = infects T cells = disable immune system
causes many symptoms (AIDs = Acquired immunodeficiency syndrome |
| How does HIV affect the body? (5) | affects T cells
clinical latency: inactive period = infected T cell reproduce
lysogenic cycle: active = destroys T cells
= less antibiodies made = less immunity
easily infected |
| How is HIV spread? (5) | sexual contact (use condoms)
pregnancy, childbirth, breastfeeding
drug use (injections)
occupational exposure (doctors)
Blood transfusions |
| Who are immune to HIV? | lack CD4+ receptor on T cells that HIV needs for docking |
