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Medicine phase 1 > Week 2 - Infection and the immune response > Flashcards

Week 2 - Infection and the immune response Flashcards

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
Q

structure of antibodies

A

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

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26
Q

function of dendritic cells

A

phagocytose pathogens before migrating to lymph nodes where they present antigens on their cell surface

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27
Q

describe the innate immune response

A

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

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28
Q

differences between innate and adaptive immune response

A

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

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29
Q

how does the adaptive immune response show memory

A

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

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30
Q

when is adaptive immunity triggered

A

when a pathogen evades the innate immune system for long enough to generate a threshold level of an antigen

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31
Q

steps of the adaptive response

A

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

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32
Q

antigen-presenting cells

A

dendritic cells
macrophages
B cells

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33
Q

how do macrophages and neutrophils recognise pathogens

A

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

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34
Q

what is a toll-like receptor and what does it do

A

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

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35
Q

examples of when an inflammatory response causes more harm than the agent itself may have produced

A

allergies, autoimmune diseases and chronic inflammatory conditions

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36
Q

clinical features of inflammation

A

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

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37
Q

process of acute inflammation

A

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

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38
Q

when may chronic inflammation occur

A

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

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39
Q

how do neutrophils and macrophages respond to pathogens

A

during phagocytosis, pathogens are engulfed into a plasma membrane-derived vacuole called a phagosome where there are destructive enzymes to kill

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40
Q

role of lymphatic capillaries

A

absorb excess fluid and return it to the great vessels at the root of the neck
smallest lymphatic vessel

41
Q

role of lymphatic vessels

A

remove excess fluid from tissues of the body

42
Q

where are lymphatic vessels found

A

throughout body apart from central nervous system and eyes

very little found in bones

43
Q

where does the lymph of the lower body return to

A

thoracic duct

44
Q

where does the lymph from lower body go after the thoracic duct

A

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
Q

how is the flow of lymph controlled

A

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
Q

where does the lymph of the upper body (head, right side of chest, neck and each upper limb) go

A

local lymphatic ducts take lymph to the union of the internal jugular vein

47
Q

lymphodema

A

damaged lymphatic vessels do not repair well and so fluid cannot drain away causing swelling

48
Q

cause of secondary lymphoma

A

develops in people who previously had a normal lymphatic system that has become damaged

49
Q

cause of primary lymphodema

A

mutations in the genes responsible for the development of the lymphatic system - fluid does not drain properly - often runs in families

50
Q

how can cancer treatment cause lymphodema

A

lymph glands are removed and radiotherapy can damage vessels and lead to lymphodema

51
Q

how is lymph cleaned in the lymphatic vessels

A

filters called lymph nodes filter out bacteria, tumour cells etc. - sometimes not all tumour cells are filtered leading to metastasis

52
Q

what are the principle lymph nodes and where are they located

A

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
Q

what is lymph

A

water, proteins, salts, lipids, white blood cells, and other substances that must be returned to the blood

54
Q

clinical features of lymphodema

A

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
Q

how does lymphatic fluid build up in tissue

A

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
Q

microbiology

A

study of microorganisms and their relationship with humans

57
Q

cellular microorganisms

A

bacteria, fungi, protozoa/other parasites

58
Q

acellular microorganisms

A

viruses, prions

59
Q

describe a prokaryote

A 
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
Q

describe a eukaryote

A

DNA on chromosomes in membrane-bound nucleus
transcription and translation are compartmentalised
cytoplasm is rich in membrane-bound organelles
80S ribosomes

61
Q

classes of bacteria

A

gram-positive
gram-negative
gram-variable
gram-stain unreliable

62
Q

process of gram staining bacteria

A

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
Q

colours of the bacteria in each step of gram staining

A

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
Q

difference between gram -ve and gram +ve bacteria

A

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
Q

how are gram-stain unreliable bacteria detected

A

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
Q

different shapes of bacteria

A

cocci, diplococcic, bacilli (rod), coccobacilli and spirochetes

67
Q

structure of bacteria

A

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
Q

colonisation

A

successful immigration where a population becomes integrated into a local community - spread to a new area but does not cause harm

69
Q

sterile body sites

A

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
Q

non sterile body sites

A

nose, throat, large intestine, vagina, uretha, skin, mouth

71
Q

virulence factors

A

mechanisms that the bacteria use to cause damage and problems for human host

72
Q

three main classes of parasites in humans

A

protozoa, helminths and ectoparasites

73
Q

opportunistic infection

A

infections that occur more often or are more severe in people with weakened immune systems than in people with healthy immune systems

74
Q

nosocomial infection

A

hospital acquired infections

75
Q

locations for bacteria to enter the body

A

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
Q

what are toxins

A

bacterial products that directly harm tissue or trigger destructive biological activities

77
Q

endotoxins

A

bacterial toxins consisting of lipids that are located within cell wall of gram negative bacteria

78
Q

exotoxins

A

toxic substances secreted by bacteria and released outside of cell

79
Q

common pathogens and their infection

A

streptococcus pneumoniae - pneumonia

staphylococcus aureus - cellulitis, septic arthritis and osteomyelitis

80
Q

normal flora

A

microorganism’s living on body but not causing disease

81
Q

course of bacterial infection

A

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
Q

infection control precautions

A

hand washing, PPE, environmental cleaning, injury prevention
care with body fluids, broken skin and mucous membranes
breaking chain of infection

83
Q

three stages of sepsis

A

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
Q

cause of ebola and route of transmission

A

caused by a virus which lives in bats and is transmitted by body fluid

85
Q

affects of ebola on body

A

virus triggers a hemorrhagic fever

blood vessels burst causing internal bleeding

86
Q

routes for intervention of ebola

A

vaccine
antibody based therapies
drugs with antibodies that bind to virus

87
Q

transmission of Zika virus

A

mosquitoes

can also enter through pregnant mother and can cause babies to be born with microcephaly

88
Q

symptoms and affects of Zika virus

A

asymptomatic in some, flu symptoms in others

may later in life develop into Guillian-bare syndrome which breaks down parts of the nervous system

89
Q

affects of malaria on body

A

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
Q

chagas disease transmission

A

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
Q

affects of chagas disease

A

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

92
Q

preventing cholera

A

purify water - boil or filter
avoid salad and any food that may have been washed
vaccine

93
Q

affects of cholera

A

gets into intestine and causes a leakage of body fluids into the intestine and very serious diarrhoea - can dehydrate very quickly

94
Q

cause of cholera

A

bacterial disease spread through contaminated water

95
Q

common gram +ve cocci

A

staphylococcus aureus

streptococcus pneumoniae

96
Q

what type of bacteria are listeria monocytogenes and corynebacterium diphtheriae

A

gram +ve rods

97
Q

common gram -ve cocci

A

neisseria meningiditis

98
Q

common gram -ve rods

A

e.coli

Medicine phase 1 (14 decks)

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