Week 2 - Infection and the immune response Flashcards

(98 cards)

1
Q

name the five WBCs

A

neutrophils, basophils, eosinophils, lymphocytes, monocytes

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2
Q

function of a neutrophil

A

as part of innate immune response they ingest and destroy invading microorganisms in tissues

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3
Q

function of a eosinophil

A

phagocytic with an affinity for antigen-antibody complexes

involved in innate and adaptive response

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4
Q

function of a monocyte

A

cytokine production - stimulated by recognition of pathogens
phagocytosis of cells
antigen presentation
form macrophages and dendritic cells

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5
Q

3 granulocytes

A

neutrophils, basophils, eosinophils - all contain granules

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6
Q

structure of a neutrophil

A

cytoplasm contains 3 types of membrane bound vesicles, secretory vesicles and granules
multi lobed nucleus (3-5)

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7
Q

structure of eosinophils

A

bilobed nucleus and contain strongly eosinophilic granules

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8
Q

structure of a basophil

A

large, intensely basophilic, cytoplasmic granules
Highly specific membrane receptors
bilobed nucleus

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9
Q

how does a cytotoxic T cell induce apoptosis

A

cell puts perforin into the cell membrane and then injects granzymes from the cell itself and these granzymes induce apoptosis

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10
Q

two types of t lymphocytes

A

helper cells (CD4+) and cytotoxic cells (CD8+)

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11
Q

function of b lymphocytes

A

produce antibodies

can become a plasma cell

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12
Q

macrophage function

A

phagocytosis of infecting microbes, antigen presentation, and general removal of dying or damaged host cells

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13
Q

what is the complement system

A

collection of plasma proteins and molecules which work together to complement killing activity of our immune system

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14
Q

three complement pathways

A

classical - activated by antigen/antibody complexes
mannose-binding lectin pathway - lectin binding to pathogen surfaces
alternative - pathogen surfaces

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15
Q

what does the complement pathway result in

A

recruitment of inflammatory cells
opsonisation of pathogens (coating surface with complement molecules)
killing of pathogens

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16
Q

location of adaptive response

A

lymphoid organs

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17
Q

function of primary lymphoid organs and examples

A

bone marrow and thymus
B lymphocytes produced and mature in bone marrow with further maturation in the spleen/lymph node
T lymphocyte precursors from bone marrow mature in the thymus

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18
Q

secondary lymphoid organ examples

A

lymph nodes and spleen

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19
Q

role of thymus

A

T cell development - precursor from bone marrow goes to the thymus to become helper or killer cells

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20
Q

role of lymph nodes

A

lymph drains from tissues
collects antigen from periphery
site of adaptive response activation
separates t and B cells in compartments (come together later)

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21
Q

role of spleen

A

filters the blood - antigens or pathogens in blood will be sieved out here
reservoir of RBCs and WBCs
collects blood-borne antigens

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22
Q

what is an MHC (major histocompatibility complex) antigen

A
molecules on the surface of the antigen presenting cell
class one - presents antigen to cytotoxic cells
class 2 - presents to helper cells
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23
Q

function of helper T cells

A

when they recognise antigen or pathogen they help by activating macrophage or B cell
can kill infected host cells

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24
Q

antibodies function

A

neutralises, opsonises and activates complement
Secreted into circulation by plasma cells, antibody then binds to pathogen and neutralises it and tries to eliminate it
antibodies can also coat the bacterial wall (similar to complement) or they can just activate complement

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25
structure of antibodies
five different antibody flavours all with the same function (IgA, IgG, IgD, IgM, IgE) - all made up of a basic IgG molecule light chain sticky and specific to a particular antigen
26
function of dendritic cells
phagocytose pathogens before migrating to lymph nodes where they present antigens on their cell surface
27
describe the innate immune response
phagocytes identify pathogen by recognising PAMPs using PRRs - they kill pathogen and digest it down to its component proteins phagocytes present the digested protein antigens to cells of adaptive response via MHCs
28
differences between innate and adaptive immune response
adaptive shows memory innate occurs locally - adaptive occurs at lymphoid organs innate is a fast response where as adaptive can take days/weeks innate involves phagocytes, NK cells, dendritic cells, mast cells whereas adaptive has T cells, B cells and antigen presenting cells
29
how does the adaptive immune response show memory
b and T cells can create memory cells to defend against future attacks of the same pathogen - a strong and faster response would be reached next time
30
when is adaptive immunity triggered
when a pathogen evades the innate immune system for long enough to generate a threshold level of an antigen
31
steps of the adaptive response
antigen for the pathogen is taken up by an antigen presenting cell APC travels to part of body containing immature t and B cells (eg lymph node) Antigen is processed by the APC and is bound to MHC receptors which presents the antigen to the T cells t cells mature and proliferate, helper T cells activate B cells which produce antibodies while killer T cells destroy pathogens that bear the antigen that was presented to them memory t and B cells are formed after infection ends
32
antigen-presenting cells
dendritic cells macrophages B cells
33
how do macrophages and neutrophils recognise pathogens
receptors on cell surface such as pattern recognition receptors (PRRs) (eg. toll-like receptors) recognise components of pathogens or other components of immune system such as complement receptors and initiate phagocytosis
34
what is a toll-like receptor and what does it do
recognises conserved patterns on pathogens and within pathogens number of different ones but they all recognise PAMPs when the receptor recognises the PAMP it initiates an inflammatory response
35
examples of when an inflammatory response causes more harm than the agent itself may have produced
allergies, autoimmune diseases and chronic inflammatory conditions
36
clinical features of inflammation
redness (rubor) – small blood vessel dilation heat (calor) – increased blood flow to vasodilation and fever swelling (tumor) – fluid in extracellular matrix pain (dolor) – stretching of tissue due to oedema, mediators such as bradykinin and serotonin stimulate pain receptors loss of function (function laesa) – movement inhibited by pain and severe swelling immobilises area
37
process of acute inflammation
vasoconstriction to minimise blood loss vasodilation increased vascular permeability as a direct result of the realise of histamine from mast cells increased blood flow and vascular permeability can dilute toxins and bacterial products at site of injury/infection - these also are associated with an influx of phagocytes at site
38
when may chronic inflammation occur
when acute inflammation is unable to clear an infectious pathogen also maybe be involved in the progression of degenerative neurological diseases, heart disease and metastatic cancer
39
how do neutrophils and macrophages respond to pathogens
during phagocytosis, pathogens are engulfed into a plasma membrane-derived vacuole called a phagosome where there are destructive enzymes to kill
40
role of lymphatic capillaries
absorb excess fluid and return it to the great vessels at the root of the neck smallest lymphatic vessel
41
role of lymphatic vessels
remove excess fluid from tissues of the body
42
where are lymphatic vessels found
throughout body apart from central nervous system and eyes | very little found in bones
43
where does the lymph of the lower body return to
thoracic duct
44
where does the lymph from lower body go after the thoracic duct
makes its way up the chest, behind oesophagus and passes into the place for the left internal jugular vein, meets the subclavian vein and enters bloodstream
45
how is the flow of lymph controlled
when you breathe in, pressure falls in the thorax and rises in the abdomen and that encourages the fluid to go into thoracic duct valves in lymphatic vessels prevent back flow when muscles contract, the tissues press on the lymphatic vessels which moves fluid along
46
where does the lymph of the upper body (head, right side of chest, neck and each upper limb) go
local lymphatic ducts take lymph to the union of the internal jugular vein
47
lymphodema
damaged lymphatic vessels do not repair well and so fluid cannot drain away causing swelling
48
cause of secondary lymphoma
develops in people who previously had a normal lymphatic system that has become damaged
49
cause of primary lymphodema
mutations in the genes responsible for the development of the lymphatic system - fluid does not drain properly - often runs in families
50
how can cancer treatment cause lymphodema
lymph glands are removed and radiotherapy can damage vessels and lead to lymphodema
51
how is lymph cleaned in the lymphatic vessels
filters called lymph nodes filter out bacteria, tumour cells etc. - sometimes not all tumour cells are filtered leading to metastasis
52
what are the principle lymph nodes and where are they located
Axillary lymph nodes – under the arm Cervical lymph nodes – neck region Supraclavicular lymph nodes – along the clavicle (collar bone) Mesenteric lymph nodes – lower abdomen Mediastinal lymph nodes – behind the sternum Inguinal lymph nodes – upper thigh region
53
what is lymph
water, proteins, salts, lipids, white blood cells, and other substances that must be returned to the blood
54
clinical features of lymphodema
Swelling of part or all of your arm or leg, including fingers or toes A feeling of heaviness or tightness Restricted range of motion Aching or discomfort Recurring infections Hardening and thickening of the skin (fibrosis)
55
how does lymphatic fluid build up in tissue
from the hydrostatic pressure and osmotic pressure exerted on the capillaries - pushes the fluid out between gaps in endothelial cells or from protein leakage
56
microbiology
study of microorganisms and their relationship with humans
57
cellular microorganisms
bacteria, fungi, protozoa/other parasites
58
acellular microorganisms
viruses, prions
59
describe a prokaryote
``` no membrane bound nucleus transcription/translation coupled single, circular chromosomal DNA additional DNA carried in plasmids 70S ribosome made up of 30S and 50S subunits ```
60
describe a eukaryote
DNA on chromosomes in membrane-bound nucleus transcription and translation are compartmentalised cytoplasm is rich in membrane-bound organelles 80S ribosomes
61
classes of bacteria
gram-positive gram-negative gram-variable gram-stain unreliable
62
process of gram staining bacteria
bacteria is fixed to slide slide is flooded with crystal violet and iodine an acid toner or alcohol based agent decolourises the gram negative counterstained with an agent such as safranin so we can see bacteria under microscope (stains gram -ve pink)
63
colours of the bacteria in each step of gram staining
blue/purple when stained with crystal violet iodine stains purple gram -ve is decolourised by an agent such as acid toner safranin stains -ve pink whereas gram +ve will stay purple
64
difference between gram -ve and gram +ve bacteria
gram positive have a thick peptidoglycan layer in their cell wall where as gram negative have a reduce peptidoglycan layer surrounded by an outer membrane that includes lipopolysaccharides and lipoproteins
65
how are gram-stain unreliable bacteria detected
very small bacteria with an atypical life cycle, atypical structure or without a complex cell wall cannot be detected by gram staining so other methods such as PCR can be used
66
different shapes of bacteria
cocci, diplococcic, bacilli (rod), coccobacilli and spirochetes
67
structure of bacteria
capsule - tough polysaccharide layer that prevents it from being englufed flagellum - allows movement through propulsion chromosome (DNA) is loosely organised in cytoplasm mesosomes - infolding that create a layer surface area for respiration plasmids - short pieces of circular DNA that replicate independently pili - hair-like and are present on surface of bacteria tp help bacteria help to each other or other structures
68
colonisation
successful immigration where a population becomes integrated into a local community - spread to a new area but does not cause harm
69
sterile body sites
blood, tissues, CNS, lower respiratory tract, organ systems , sinuses, inner and middle ear, renal system down to posterior uretha, female reproductive tract down to cervix, eye
70
non sterile body sites
nose, throat, large intestine, vagina, uretha, skin, mouth
71
virulence factors
mechanisms that the bacteria use to cause damage and problems for human host
72
three main classes of parasites in humans
protozoa, helminths and ectoparasites
73
opportunistic infection
infections that occur more often or are more severe in people with weakened immune systems than in people with healthy immune systems
74
nosocomial infection
hospital acquired infections
75
locations for bacteria to enter the body
skin with cut or tear, the mouth, nose, respiratory tract, ears, eyes, urogenital tract, anus, GI tract can enter bloodstream or peritoneum through a break in the normal barrier
76
what are toxins
bacterial products that directly harm tissue or trigger destructive biological activities
77
endotoxins
bacterial toxins consisting of lipids that are located within cell wall of gram negative bacteria
78
exotoxins
toxic substances secreted by bacteria and released outside of cell
79
common pathogens and their infection
streptococcus pneumoniae - pneumonia | staphylococcus aureus - cellulitis, septic arthritis and osteomyelitis
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normal flora
microorganism's living on body but not causing disease
81
course of bacterial infection
Penetration - break in epithelium, pili adhere to surfaces Colonisation - uses nutrients from environment, replicates Tissue destruction - releases degradative enzymes, release toxins (either endo or exo) - Body response - WBCs and antibodies respond, pus formed from dead neutrophils
82
infection control precautions
hand washing, PPE, environmental cleaning, injury prevention care with body fluids, broken skin and mucous membranes breaking chain of infection
83
three stages of sepsis
sepsis severe sepsis - sepsis with evidence of organ hypoperfusion (inadequate delivery of oxygen and nutrients) septic shock - severe sepsis with hypotension (low bp) despite fluid resuscitation or vasopressor/inotropic support
84
cause of ebola and route of transmission
caused by a virus which lives in bats and is transmitted by body fluid
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affects of ebola on body
virus triggers a hemorrhagic fever | blood vessels burst causing internal bleeding
86
routes for intervention of ebola
vaccine antibody based therapies drugs with antibodies that bind to virus
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transmission of Zika virus
mosquitoes | can also enter through pregnant mother and can cause babies to be born with microcephaly
88
symptoms and affects of Zika virus
asymptomatic in some, flu symptoms in others | may later in life develop into Guillian-bare syndrome which breaks down parts of the nervous system
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affects of malaria on body
parasites first invade liver then turn into another form and escape into red blood cells – parasites erupt out of red blood cells every few days resulting in a fever – repeats In falciparum Malaria, the parasites make the red blood cells sticky, and that's to stop them getting recognised in your spleen - can then get caught in blood vessels and if this prevents oxygen getting to brain it can cause cerebral malaria and death
90
chagas disease transmission
triatomine bug sucks your blood while you're asleep and leaves their faeces (parasite located in here) on you which causes you to itch - end up rubbing parasite into your lips allowing it to enter
91
affects of chagas disease
acute response then a 15 year ish phase of no symptoms - after this period you may die of a massive heart attack of hugely expanded oesophagus or colon bc parasites have stayed there
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preventing cholera
purify water - boil or filter avoid salad and any food that may have been washed vaccine
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affects of cholera
gets into intestine and causes a leakage of body fluids into the intestine and very serious diarrhoea - can dehydrate very quickly
94
cause of cholera
bacterial disease spread through contaminated water
95
common gram +ve cocci
staphylococcus aureus | streptococcus pneumoniae
96
what type of bacteria are listeria monocytogenes and corynebacterium diphtheriae
gram +ve rods
97
common gram -ve cocci
neisseria meningiditis
98
common gram -ve rods
e.coli