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micro orgamisims Flashcards

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1
Q

microrganisims

A

essential for decomposition/ recycle nutrients

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2
Q

prokaryote vs eukaryote

A

pro- lack nucleus/ have free floating DNA, undergo asexual reproduction ( binary fusion )/ unicellular

euk- multicelluar, membrane bound organells, nucleus, sexual reproduction ( mitosis )

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3
Q

virus

A

not living
no cellular strucute
protein coat around the DNA or RNA
can mutate
antibiotics are innefective antivirals required

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4
Q

bacteria

A

prokaryotic
unicellular
have a cell wall

e.coli
gastrointestianal tract bacteria
syphylisis

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5
Q

protazoa

A

eukaryotic
no cell wall
drugs are usually more toxic b/c damaging same cells as human\
motoz- move around
malaria

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6
Q

fungi

A

eukaryotic
antifungals
have a cell wall
produce spores- how they reproduce
ringworm tinea

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7
Q

helminths

A

eukaryotic
multicellular
eggs, larva, then develop into adult
don’t proliferate the host

tapeworm

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8
Q

bacteria optimum temperature

A

37 degrees

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9
Q

bacteria optimum PH

A

7

exceptions- bacteria in stomachs

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10
Q

3 types of bacteria

A

oligate arobes- oxygen only grow in presence in oxygen

oligate anerobes- can only grow in prsence of no oxygen

faculative anerobes - both conditions

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11
Q

gram positive bacteria

A

thick layer of peptidoglycan
can form spores- survive harsh conditions so will cause
reinfection

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12
Q

gran negative bacteria

A

reinforced with second membrane
more difficult to kill
produce endotoxins

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13
Q

microbiota

A

normal flora

work in symbiotic relationship with the human body to help the body

prevent bad bacteria from gorwing, take up space, nutrients
reduce PH, outcompete other pathogens, syntehsise important nutrients
could prevent normal cells from growing
could transfer antibiotice resistance to bad bacteria
use gloves to prevent

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14
Q

mode of transmission

A

contact= contact between 2 people by touch

vichele- using air, water, food

vector- transfer of pathogen via an animal

fomite- born= by air or inanimate object

vertical- through the placenta so mum to child

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15
Q

chain of infection

A

infectious agent- reservoir ( population that the infectious agent sits ) - portal of entry ( how it enters )- mode of transmision ( how it transmits to each patient ) - point of exit ( how it leaves )- suseptible host ( contract disease, people with low immune systems )

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16
Q

enviroment control

A

steralisation

disinfection

sanitation

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17
Q

steralisation

A

destrcution/ elimination of all microbes

heat - glass wear
radiation - heat sensitive matirial
filitration- protein solutions
chemical - bleach- metal implements

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18
Q

disinfection

A

elimination of most pathogens from inanimate object

chemical- alcohol
gas-

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19
Q

sanitation

A

safe disposial of human waste- e.g urine, blood

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20
Q

requirements for disease

A

Pathogenicity – the ability of a microbial agent to cause disease

Virulence – the degree to which an organism is pathogenic- ability to cause

Sufficient dose
Portal of entry and exit: breach host defences

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21
Q

pathogenic properties

A

Adherence
Adhesion is the capability of pathogenic microbes to attach to the cells of the body using adhesion factors

Invasion is the ability of a pathogen to enter host cells or tissues, spread and cause disease.

Toxins
In addition to enzymes, certain pathogens are able to produce toxins, biological poisons that assist in their ability to invade and cause damage to tissues

Evasion

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22
Q

Adherance

A

Adhesins are found on the surface of certain pathogens and bind to specific receptors on host cells, for example on;

fimbriae and flagella of bacteria
cilia of protozoa
capsids or membranes of viruses

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23
Q

invasion

A

Glycohydrolases- Degrades hyaluronic acid that cements cells together to promote spreading through tissues

nucleases- Degrades DNA released by dying cells

Phospholipase- Degrades phospholipid bilayer of host cells

protease- Degrades collagen in connective tissue to promote spread

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24
Q

toxins

A

endotoxins- gram negative bacteria- resulting in the disintegration of the membrane

exotoxins- gram positive bacteria and gram negative
Exotoxin targets specific receptors on specific cells and damages those cells through unique molecular mechanisms.

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25
antigen
can initiate an immune response identified as foreign
26
inate immune response
non-specific react same to every pathogen inborn 1st and 2nd line of defense
27
adaptive/ aquired
specific against one specific pathogen developed over time require exsposure 3rd line of defense
28
first line of defense
inate/ non specific protect portal of entry keep every invader out and prevent infection Barriers ( physical, chemical ) physical- intact barrier/ structure- skin, chemical- mucous membrane/ hair and cilia fluids- tears, saliva, acid defaction/ vommiting
29
second line of defense
inate/ non specific antimicrobial chemicals phagocytes natural killer cells inflamtion fever
30
antimicrobial second line of defesne
interferon= inteferes with viral infection and activates immune cells... will flag for destruction complement proteins- will bind to anything forigen= so will highlight it and will flag pagocytes to destroy it.
31
phagocytes second line of defense
chemotaxins will flag phagocytes phagocytosis occurs, 1. phagocyte will recognise pathogen as forign 2. pahgocyte will engulg the pathogen and form a phaosome 3. lysosome in the cell will then merge and bind with phagosome forming a phagolysosome 4. lysomome contains digestive enzymes which will break down pathogen 5. exocytosis will occur
32
natural killer cells second line of defense
target abnormal cells will attack pre cancerous cells
33
inflamation second line of defense
to limit chances of infections at this wound damaged cells will see MAST cells release histamine and causes pahgocytes to come to the site. increased blood flow// increased leakage traps the pathogen from entering the blood stream remove dead tissue because it will stop healing 1. redness- increase blood flow for phagocytosis 2. heat- increase blood flow 3. swelling- capilary permability increase fluid leakage- increase phagocytosis 4. pain 5. loss of function in this site
34
fever 2nd line of defense
systemic response increase temp to increase immune cell functions decrease the pathogen functions higher metabolic rate to increase healing
35
two adaptive immune responses
cell-mediated antibody- mediated specific/ versatile/ memory/ tolerance/ memory
36
cell mediated response third line of defense
T cell kill directly and don't make antibodies T CELL activation= MHC marker on the surface of T cell- the antigen will bind to this CD4- prsented on T helper cell CD8 - T killer cells
37
MHC 1
For a T cell to recognize an antigen, the antigen must be bound to Major Histocompatibility Complex (MHC) in the PM of another cell so will display the non-self antigen on MHC 1 marker to have it destroyed thus activate cytoxic T cells to destroy by releaseing toxins
38
MHC 2
Antigen presenting cell (APC): Macrophage, Lymphocyte B or dendritic cells, express MHC 2 Helper T cell (via CD4 receptor) recognise foreign II MHC 7. Helper T cells secrete cytokines A. Attract and stimulate macrophages B. Attract and stimulate cytotoxic T cells C. Promote activation of B cells → make antibodies
39
helper T cells
ACTIVATED by pathogens actract macrophages or activate B cells
40
antibody
plasma cells secrete antibodies long protein chain- heavy and a light chain constant region- Ige antibodies have the same variable region changes depending on the shape of the antigen binding site
41
types of antibody
IgA- on muscosa/ blood IgE- activate in allergies IgD- B cell surface IgG- memory IgM- first made
42
antibody - mediated response
Defend against antigens and pathogens * B cell doesn’t directly touch antigen * Produce antibodies (immunoglobulin) * Provides immunological memory * React instantly next time it sees the same enemy
43
antibodies
Activation of complement 2. Attraction of phagocytes 3. Stimulation of inflammation 4. Prevention viral/bacterial adhesion 5. Precipitation and agglutination 6. Neutralisation 7. Opsonisation
44
4 types of immunity
active or passive (memory) natural or artificial
45
natural
come into contact with the disease
46
artificial
immunisation- given a vaccine/ the disease
47
immunisation
body will make antibdies against antigen memory cells made destroy if re-exsposed secondary response- quicker/ more rapid and a greater concentration of antibodies are produced because of the B cells already being present
48
vaccine pros/ cons
pros= Protective for relevant disease * Safe * No adverse effects * Sustained * Long-term protection * Generate antibodies (B cells) or protective T cells * Practical * Use and stability cons= Adverse reactions * Redness and swelling * Allergic reactions * Consider * Prevalance of disease * Severity of disease * Morbidity and mortality
49
herd immunity
85 percent of immunity will protect the entire population decreases the number of hosts able to pass on disease
50
nosocomial infection
an infection that you get in a hospital
51
acute inflamation
remove injuury agents remove infectious agent clear damaged cells innate
52
chronic inflammation
if acute goes on for a long time auto-immune
53
purpose of inflammation
destroys, dilutes, neutralises disease agents stimmulate immune response enable healing
54
chemical inflammation
cells that are damaged will release histamine histamine will increase capilary permability prostaglandis- vasodilation thromboxanes- clotting leukotrines- attract wbc
55
two types of inflamtion
vascular phase cellular phase
56
vascular phase of inflammation
vasodilation increased blood flow to site of injury redness and heat increased vascular permability - swelling protein rich plasma leaves the blood vessels
57
exudate vs transudate
rich in protein fibrin present increased vascular permability
58
cellular phase
Margination and adhesion. 2. Transmigration or Diapedesis. 3. Chemotaxis. 4. Activation of leukocytes  phagocytosis
59
inflammation signs cardinal
redness warmth pain swelling loss of function
60
systemic effects of inflammation
fever aneorexia leukocytosis malasise
61
aged effects to inflammation
longer onset less dendritic cells NK cells less toxic decline in phagocytosis

Biology (19 decks)

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