communicable diseases, disease prevention and immune system Flashcards

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1
Q

whats a primary response

A

first line of defense to keep pathogens out of the body

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2
Q

how does skin keep pathogens out

A

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

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3
Q

how do mucous membranes keep pathogens out

A

goblet cells - secrete mucus to trap pathogens

cilia - waft mucus up and out of trachea to be digested

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4
Q

what are lysozymes and how do they keep pathogens out

A

enzymes found in urine and tears

they hydrolise macromolecules in pathogens

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5
Q

expulsive reflexes and how do they keep pathogens out

A

vomiting coughing sneezing etc

eject pathogen laden material away from body

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6
Q

blood clotting process

A

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

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7
Q

what is secondary defense

A

responses once pathogen is inside body

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8
Q

how does inflammation work

A

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

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9
Q

what are phagocytes

A

specialised wbc that engulf and destroy pathogens

two types: neutrophils and macrophages

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10
Q

describe and explain function of the two types of phagocytes

A

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

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11
Q

outline the process of phagocytosis

A
  1. pseudopods extend to surround pathogen
  2. pseudopods fuse to form a vesicle
  3. pathogen is engulfed forming a phagosome
  4. lysosome fuses w phagosome forming a phagolysosome
  5. hydrolisis of macromolecules in pathogen occurs
  6. simple molecules absorbed into cytoplasm, waste products removed via exocytosis
  7. antigens retained on cell surface membrane, becomes an antigen presenting cell alerting other cells of the attack
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12
Q

what are opsonins

A

chemicals that bind to pathogens and “tag” them so they can be recognised more easily by phagocytes for phagocytosis

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13
Q

what are antigens

A

usually polysaccharides/proteins, antigens trigger an immune response which involves production of antibodies

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14
Q

the specific immune response - B-cells

A

develop in bone marrow

  1. b-lymphocyte’s antibody binds with a complementary antigen
  2. clonal selection and proliferation- b-lymphocyte multiplies many times (clonal expansion)
  3. 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

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15
Q

the specific immune response - T-cells

A

develop in the thymus

  1. an antigen presenting cell (macrophage) ingests, processes and presents antigen
  2. T-helper lymphocyte or T-killer lymphocyte binds to complementary antigen on APC
  3. clonal selection and proliferation- one clone stimulated and T-lymphocyte divides many times
  4. 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

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16
Q

in clonal expansion, lymphocytes divide by ____

A

mitosis

17
Q

what is cell signalling

A

cells communicating with each other to co-ordinate their responses

18
Q

what are monokines

A

a type of cytokines released by macrophages, they attract neutrophils for phagocytosis

19
Q

what are interleukins

A

a type of cytokines released by T-helper cells, they stimulate clonal expansion and differentiation of B and T-lymphocytes

20
Q

what is an autoimmune disease

A

immune system doesn’t recognise its own antigens and attacks the organism’s own healthy tissues

21
Q

examples of autoimmune diseases

A

rheumatoid athritis- affects connective joints
lupus - affects nervous system

neither have a cure, can be managed with anti-inflammatory drugs, steroids, immunosuppressant drugs

22
Q

what are antibodies

A

glycoproteins (amino acids+sugars), known as immunoglobulins,
each contain a variable region which is specific to an antigen

23
Q

structure of an antibody

A

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)

24
Q

what are agglutins

A

agglutins glue pathogens together, slowing the rate of pathogens and makes phagocytosis faster

25
Q

anti-toxins

A

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

26
Q

similarities and differences betw primary and secondary responses

A

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

27
Q

what is passive and active immunity

A

active - body makes its own antibodies

passive - body obtains antibodies from other individuals, eg breastmilk, vaccines

28
Q

types of vaccines

A

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

29
Q

why are vaccines injected

A

pH and protease in stomach would otherwise denature and dismantle antigens

30
Q

how can an antigenic shift occur

A

individual mutation (viruses prone to mutation) –> rapid generational growth (viruses reproduce fast) –> increase of new strains

31
Q

how can an epidemic/pandemic be avoided

A

reduce rate of transmission eg. lockdown
vaccinations
program of economic aid
global monitoring of variants

32
Q

how can antibiotic resistance be minimised

A
  1. prevent infection - covering wounds, cleaning, PPE
  2. diagnose effectively - preferably before treatment, modern rapid DNA testing doesn’t require waiting for bacteria to grow overnight
  3. optimise use of antibiotics - take whole course, only when needed, don’t use in animal feed
  4. prevent transmission - effective handwashing and disinfecting, care with raw meat etc
33
Q

how can a micro-organism become antibiotic resistant

A
  1. random genetic mutation makes it resistant
  2. bacteria exposed to antibiotics (selective pressure)
  3. resistant bacteria survive
  4. reproduce and pass on the allele for antibiotic resistance
  5. frequ of allele for resistance increases and resistance will be more common in population