communicable diseases, disease prevention and immune system Flashcards
whats a primary response
first line of defense to keep pathogens out of the body
how does skin keep pathogens out
keratinised cells - are dry and are constantly shed and replaced
normal flora - natural ecosystem of bacteria and fungi outcompete potential pathogens
sebum - acts as a natural antioxidant
how do mucous membranes keep pathogens out
goblet cells - secrete mucus to trap pathogens
cilia - waft mucus up and out of trachea to be digested
what are lysozymes and how do they keep pathogens out
enzymes found in urine and tears
they hydrolise macromolecules in pathogens
expulsive reflexes and how do they keep pathogens out
vomiting coughing sneezing etc
eject pathogen laden material away from body
blood clotting process
injured platelets and tissue release clotting factor prothrombin activator and calcium ions
prothrombin activator converts prothrombin –> thrombin
thrombin splits fibrinogen –> fribrin
fibrin forms a mesh over wound trapping platelets and rbc
enzyme plasmin is used to dissolve the clot
what is secondary defense
responses once pathogen is inside body
how does inflammation work
mast cells release cytokines and histamines
histamines signal cells of capillary endothelium to become more permeable
cytokines attract phagocytes
capillary widening –> increased blood flow
increased capillary permeability –> release of tissue fluid
what are phagocytes
specialised wbc that engulf and destroy pathogens
two types: neutrophils and macrophages
describe and explain function of the two types of phagocytes
neutrophils - multi-lobed, small, short lived, produced in large amounts in response to an infection,
contain lysosomes, engulf and digest pathogens and die shortly after, collected as pus
macrophages - larger than neutrophils, do not fully digest pathogens but display part of the pathogen on its membrane, becoming an antigen presenting cell
outline the process of phagocytosis
- pseudopods extend to surround pathogen
- pseudopods fuse to form a vesicle
- pathogen is engulfed forming a phagosome
- lysosome fuses w phagosome forming a phagolysosome
- hydrolisis of macromolecules in pathogen occurs
- simple molecules absorbed into cytoplasm, waste products removed via exocytosis
- antigens retained on cell surface membrane, becomes an antigen presenting cell alerting other cells of the attack
what are opsonins
chemicals that bind to pathogens and “tag” them so they can be recognised more easily by phagocytes for phagocytosis
what are antigens
usually polysaccharides/proteins, antigens trigger an immune response which involves production of antibodies
the specific immune response - B-cells
develop in bone marrow
- b-lymphocyte’s antibody binds with a complementary antigen
- clonal selection and proliferation- b-lymphocyte multiplies many times (clonal expansion)
- differentiation into memory cells or plasma cells which secrete large amounts of antibody
if antigen appears later the memory cells are stimulated , divide and produce many plasma cells quickly
the specific immune response - T-cells
develop in the thymus
- an antigen presenting cell (macrophage) ingests, processes and presents antigen
- T-helper lymphocyte or T-killer lymphocyte binds to complementary antigen on APC
- clonal selection and proliferation- one clone stimulated and T-lymphocyte divides many times
- differentiates into either T-killer or T-helper
T-killer - bind to cells presenting complementary antigen and kills them
T-helper - secrete cytokines which stimulate phagocytes and other lymphocytes
in clonal expansion, lymphocytes divide by ____
mitosis
what is cell signalling
cells communicating with each other to co-ordinate their responses
what are monokines
a type of cytokines released by macrophages, they attract neutrophils for phagocytosis
what are interleukins
a type of cytokines released by T-helper cells, they stimulate clonal expansion and differentiation of B and T-lymphocytes
what is an autoimmune disease
immune system doesn’t recognise its own antigens and attacks the organism’s own healthy tissues
examples of autoimmune diseases
rheumatoid athritis- affects connective joints
lupus - affects nervous system
neither have a cure, can be managed with anti-inflammatory drugs, steroids, immunosuppressant drugs
what are antibodies
glycoproteins (amino acids+sugars), known as immunoglobulins,
each contain a variable region which is specific to an antigen
structure of an antibody
contains a constant region and variable region which is an antigen binding site
two heavy chains (long polypeptide) and two light chains (short polypeptide)
contains disulfide bridges (betw two cysteines)
what are agglutins
agglutins glue pathogens together, slowing the rate of pathogens and makes phagocytosis faster
anti-toxins
can be competitive/non competitive inhibitors
competitive- anti-toxins are a complementary fit to active site of toxin so the toxin can no longer bind to active site
non-competitive - complementary fit to allosteric site, changes the tertiary structure of toxin so it can no longer bind
similarities and differences betw primary and secondary responses
similarities: both have a delay, both reach a peak, both produce antibodies as a response
differences: secondary has steeper start, higher peak and slower decrease
what is passive and active immunity
active - body makes its own antibodies
passive - body obtains antibodies from other individuals, eg breastmilk, vaccines
types of vaccines
live attenuated (weakened but alive) - eg measles, tuberculosis, polio
inactivated (killed pathogen) - eg. inactivated polio virus
subunit (purified antigen) - eg. hepatitis b,
toxoid (inactivated toxins) - eg. tetanus
why are vaccines injected
pH and protease in stomach would otherwise denature and dismantle antigens
how can an antigenic shift occur
individual mutation (viruses prone to mutation) –> rapid generational growth (viruses reproduce fast) –> increase of new strains
how can an epidemic/pandemic be avoided
reduce rate of transmission eg. lockdown
vaccinations
program of economic aid
global monitoring of variants
how can antibiotic resistance be minimised
- prevent infection - covering wounds, cleaning, PPE
- diagnose effectively - preferably before treatment, modern rapid DNA testing doesn’t require waiting for bacteria to grow overnight
- optimise use of antibiotics - take whole course, only when needed, don’t use in animal feed
- prevent transmission - effective handwashing and disinfecting, care with raw meat etc
how can a micro-organism become antibiotic resistant
- random genetic mutation makes it resistant
- bacteria exposed to antibiotics (selective pressure)
- resistant bacteria survive
- reproduce and pass on the allele for antibiotic resistance
- frequ of allele for resistance increases and resistance will be more common in population
