Body defence Flashcards

1
Q

define acute inflammation

A

an immediate, adaptive response with limited specificity caused by several noxious stimuli, such as infection and tissue damage (tissue necrosis).
only lasts a short period of time

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2
Q

what is chronic inflammation

A

Your body continues sending inflammatory cells even when there is no outside danger. For example, in rheumatoid arthritis inflammatory cells and substances attack joint tissues leading to an inflammation that comes and goes and can cause severe damage to joints with pain and deformities.

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3
Q

what is acute inflammation caused by

A

Acute inflammation is typically caused by injuries, like a sprained ankle, or by illnesses, like bacterial infections and common viruses

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4
Q

5 signs of acute inflammation

A
heat
redness 
swelling
pain
loss of function
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5
Q

what is heat and redness also known as

A

hyperaemia (due to increased blood flow)

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6
Q

what is exudate

A

swelling - fluid moving from the blood flow to interstitial caused by increased blood flow

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7
Q

describe the vascular changes that happen during acute inflammation (vascular calibre, blood flow, vascular permeability)

A

vascular calibre: rapid transient (lasting only for a short time)vasoconstriction of arterioles followed by vasodilation
blood flow: initial reduction of blood flow by increased blood flow to the capillaries
vascular permeability: increased permeability of microvasculature
outpouring of protein rich fluid from the plasma - exudate
>hydrostatic pressure +

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8
Q

describe inflammatory swelling

A

is oedema due to accumulation of exudate

exudate is: inflammatory extravascular fluid - protein rich

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9
Q

describe “not” inflammatory swelling

A

is oedema due to accumulation of transudate

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10
Q

define transudate

A

Transudate is an ultrafiltrate of plasma that contains few, if any, cells and does not contain large plasma proteins, such as fibrinogen. Transudate results from increased hydrostatic or reduced oncotic pressure.

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11
Q

what is extravasation

A

where endothelial cells and leucocytes express mutually recognising adhesion molecules
Extravasation is the leakage of a fluid out of its container into the surrounding area, especially blood or blood cells from vessels. In the case of inflammation, it refers to the movement of white blood cells from the capillaries to the tissues surrounding them

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12
Q

what is migration in terms of cellular events

A

Leucocytes move following concentration gradients of chemical and inflammatory mediators (chemotaxis)

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13
Q

three stages of phagocytosis

A

recognition and adhesion
engulfment
killing or degradation

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14
Q

define pus

A

a thick yellowish or greenish opaque liquid produced in infected tissue, consisting of dead white blood cells and bacteria with tissue debris and serum.

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15
Q

define abscess

A

a swollen area within body tissue, containing an accumulation of pus.

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16
Q

define empyema

A

the collection of pus in a cavity in the body, especially in the pleural cavity.

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17
Q

three plasma mediators

A

coagulation system
kinin system
complement system

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18
Q

three cell mediators

A

mast cells
basophils
platelets

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19
Q

what are chemical mediators

A

endogenous (having an internal cause or origin.) chemical agent which takes an active part in the development of the inflammatory response.

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20
Q

what is the coagulation system activated by

A

tissue damage

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21
Q

end product of coagulation system

A

fibrin

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22
Q

what is fibrin

A

an insoluble protein formed from fibrinogen during the clotting of blood. It forms a fibrous mesh that impedes the flow of blood.

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23
Q

thrombin role in the coagulation system

A

increases leukocyte adhesion and fibroblast proliferation

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24
Q

factor Xa role in the coagulation system

A

increases vascular permeability and leukocyte exudation

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25
Q

describe the kinin system

A

(poorly understood hormonal system with limited available research. It consists of blood proteins that play a role in inflammation, blood pressure control, coagulation and pain.)
• Activated through coagulation factor XII
end product is bradykinin causing vasodilation and triggering pain

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26
Q

what’s an opsonin

A

extracellular proteins that, when bound to substances or cells, induce phagocytes to phagocytose the substances or cells with the opsonins bound. Thus, opsonins act as tags to label things in the body that should be phagocytosed by phagocytes.

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27
Q

describe the complement system

A

(The complement system, also known as complement cascade, is a part of the immune system that enhances the ability of antibodies and phagocytic cells to clear microbes and damaged cells from an organism, promote inflammation, and attack the pathogen’s cell membrane.)
triggers expression of adhesion molecules on leucocytes

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28
Q

what is a vasoactive amine

A

A substance containing amino groups, such as histamine or serotonin, that acts on the blood vessels to alter their permeability or to cause vasodilation.

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29
Q

describe histamine’(what does it contain, what is it released in response to, what does it do)

A

contain basophils, mast cells and platelets
released into response to: physical injury, trauma, cold or heat
causes dilation of arterioles and increases vascular permeability of the venules

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30
Q

describe serotonin

A

contains platelets and enterchromaffin cells

actions similar to those of histamine

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31
Q

what does arachidonic acid metabolite do as a cell mediator

A

prostaglandin, arteriolar dilatation and pain

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32
Q

what do cytokines and chemokines do as cell mediators

A

increased vascular permeability and chemotaxis

Chemotaxis is the phenomenon by which cell movement is directed in response to an extracellular chemical gradient

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33
Q

what is chemotaxis

A

Chemotaxis is the movement of an organism or entity in response to a chemical stimulus.

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34
Q

what does nitric oxide do as a cell mediator

A

vasodilation

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35
Q

what does platelet activatin factor do as a cell mediator

A

platelet aggregation
increased vascular permeability
activation of leucocytes

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36
Q

what are leukocytes

A

the cells of the immune system that are involved in protecting the body against both infectious disease and foreign invaders.
(leucocytes and leukocytes are the same thing)

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37
Q

7 systemic effects of inflammation

A
fever
malaise, lethargy, and sleepiness
pain
leucocytosis
tissue damage
swelling in a confined space
hyperpyrexia
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38
Q

what is hyperpyrexia

A

a condition where the body temperature goes above 106.7 degrees Fahrenheit (41.5 degrees Celsius) due to changes in the hypothalamus — the organ in the brain that regulates temperature.‌ Hyperpyrexia is a life-threatening emergency that demands urgent medical attention.

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39
Q

how is a fever caused during inflammation

A

IL1, IL6 and TNF cause release of prostaglandins affecting the hypothalamic thermostat with temperature being set higher.

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40
Q

how is Malaise, lethargy and sleepiness caused during inflammation

A

Cytokines affecting the brain to reduce behaviour which could be counterproductive

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41
Q

what is leucocytosis

A

A higher-than-normal number of white blood cells is called leukocytosis. Leukocytes usually increase in number when they are doing their job, but there are some other conditions that can cause an increase.

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42
Q

what is fibrinous inflammation

A

fibrinogen exits the blood and accumulate as fibrin in extracellular space, due to increased vascular permeability or procoagulant stimuli (tumours)

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43
Q

what is suppurative inflammation

A

The process of pus formation, called suppuration, occurs when the agent that provoked the inflammation is difficult to eliminate. Pus is a viscous liquid that consists mostly of dead and dying neutrophils and bacteria, cellular debris, and fluid leaked from blood vessels.

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44
Q

what is purulent inflammation

A

Production of pus, comprising neutrophils, dead or alive, cellular debris and oedema

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45
Q

difference between suppurative and purulent inflammation

A

Both purulent and suppurative are used to describe pus formation. However, others employ purulent and suppurative in a more specific way: purulent is used to describe the pus forming in the affected area whereas suppurative is used to describe the pus oozing from the site of injury or infection

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46
Q

what is death due to severe local damage called

A

meningitis

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47
Q

what is death due to uncontrollable infection called

A

sepsis and shock

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48
Q

describe the process of acute inflammation in appendicitis

A
Acute appendicitis (AA) is a suppurative inflammatory process of the vermiform appendix and is the most common life-threatening surgical emergency in the pediatric age group.
(vermiform appendix: vermiform appendix is a narrow, worm-shaped structure that protrudes from the posteromedial aspect of the cecum, 2 cm (or less) below the insertion of the ileum into the cecum)
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49
Q

what is osteomyelitis

A

a bone infection

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50
Q

what is pathogenesis

A

is the process by which a disease or disorder develops

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51
Q

pathogenesis of chronic inflammation

A

often develops during the transition from acute inflammation to tissue repair. Chronic inflammation may also develop de novo in response to certain types of insults.

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52
Q

mechanism of chronic inflammation

A

adaptive immune responses can cause ongoing and excessive activation of innate immune cells.

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53
Q

morphology of chronic inflammation

A

fairly non-specific. However, the proportions of each cell type will vary depending on the condition. For example, Plasma cells are prevalent in rheumatoid arthritis, whereas in chronic gastritis, lymphocytes are typically more abundant.

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54
Q

outcome of chronic inflammation

A

your body’s inflammatory response can eventually start damaging healthy cells, tissues, and organs. Over time, this can lead to DNA damage, tissue death, and internal scarring. All of these are linked to the development of several diseases, including: cancer.

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55
Q

diagnostic tests used to test for inflammation

A

Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are blood tests that can be used to check the levels of inflammation in your body.

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56
Q

how does ESR test for inflammation

A

The ESR rate increases as a result of any cause or focus of inflammation. When an inflammatory process is present, fibrinogen enters the blood in high amounts and causes red cells to stick to each other, which raises the ESR. Moderate elevations are common in active inflammatory diseases.

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57
Q

CRP test for inflammation

A

A high level of CRP in the blood can be a marker of inflammation. A wide variety of conditions can cause it, from an infection to cancer. High CRP levels can also indicate that there’s inflammation in the arteries of the heart, which can mean a higher risk of heart attack.

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58
Q

Long-term diseases that doctors associate with inflammation

A
asthma
chronic peptic ulcer 
tuberculosis
rheumatoid arthritis 
periodontitis
ulcerative colitis
sinusitis
active hepatitis
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59
Q

what is granulomatous inflammation

A

pecial type of chronic inflammation characterised by often focal collections of macrophages, epithelioid cells and multinucleated giant cells.

Examples of noninfectious granulomatous diseases are sarcoidosis, Crohn’s disease, berylliosis, granulomatosis with polyangiitis, eosinophilic granulomatosis with polyangiitis, pulmonary rheumatoid nodules, and aspiration of food and other particulate material into the lung.

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60
Q

how does tuberculosis cause chronic inflammationsis

A

This immune response to TB is described as a chronic granulomatous inflammation; caused by close interaction between Mtb bacilli and host immune agents at the infection site

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61
Q

what does fibrosis mean

A

thickening or scarring of the tissue.

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62
Q

what is regeneration of tissue

A

natural process of replacing or restoring damaged or missing cells, tissues, organs, and even entire body parts to full function in plants and animals

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63
Q

what is repair by fibrosis

A

Tissue repair is a protective response after injury, but repetitive or prolonged injury can lead to fibrosis, a pathological state of excessive scarring

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64
Q

liver fibrosis

A

the excessive accumulation of extracellular matrix proteins including collagen that occurs in most types of chronic liver diseases. Advanced liver fibrosis results in cirrhosis, liver failure, and portal hypertension and often requires liver transplantation.

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65
Q

what is healing by primary intention

A

is the healing that occurs when a clean laceration or a surgical incision is closed primarily with sutures, Steri-Strips, or skin adhesive.

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66
Q

what is healing by secondary intention

A

a wound will be left open (rather than being stitched together) and left to heal by itself, filling in and closing up naturally.

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67
Q

how does poor blood supply affect wound healing

A

The availability of oxygen (O2) to cells in the wound area and the presence of adequate blood flow are important factors to the healing process. Oxygen plays a critical role in the formation of collagen, the growth of new capillaries, and the control of infection.

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68
Q

how does steroid therapy affect wound healing

A

Glucocorticoids (corticosteroids) cause dehiscence (the splitting or bursting open of a pod or wound) of surgical incisions, increased risk of wound infection, and delayed healing of open wounds

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69
Q

how does diabetes mellitus affect wound healing

A

People with uncontrolled diabetes may develop poor circulation. As circulation slows down, blood moves more slowly, which makes it more difficult for the body to deliver nutrients to wounds. As a result, the injuries heal slowly, or may not heal at all.

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70
Q

how does poor nutrition affect wound healing

A

can delay healing and impair wound strength, making the wound more prone to breakdown. There is a significant body of evidence supporting the essential role of nutrition in wound healing.

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71
Q

what are decubitus ulcers

A

Bedsores — also called pressure ulcers and decubitus ulcers — are injuries to skin and underlying tissue resulting from prolonged pressure on the skin. Bedsores most often develop on skin that covers bony areas of the body, such as the heels, ankles, hips and tailbone

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72
Q

what are arterial ulcer

A

painful injuries in your skin caused by poor circulation. ‌ Arterial ulcers typically happen when blood is unable to flow into the lower extremities, like the legs and feet

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73
Q

what are venous ulcers

A

leg ulcers caused by problems with blood flow (circulation) in your leg veins. Normally, when you get a cut or scrape, your body’s healing process starts working to close the wound.

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74
Q

what is granulation tissue

A

vascularised fibrous tissue that replaces the fibrin clot and is part of the repair process

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75
Q

what do granulomas do

A

destroy or isolate pathogens or foreign material but might cause tissue destruction

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76
Q

cell renewal proliferation

A

will replace the lost cells

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77
Q

cell renewal differentiation

A

will replace complex architectural structures

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78
Q

labile cells

A

cells that continuously multiply and divide throughout life. This continual division of labile cells allows them to reproduce new stem cells and replace functional cells that are lost in the body

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79
Q

what is angiogenesis

A

formation of new blood vessels

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80
Q

innate immune response

A

the innate immune response consists of physical, chemical and cellular defenses against pathogens. The main purpose of the innate immune response is to immediately prevent the spread and movement of foreign pathogens throughout the body.

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81
Q

What is adaptive immunity

A

Adaptive immunity/acquired immunity/specific immunity

  • is specific to the pathogen presented.
  • meant to attack non-self pathogens but can sometimes make errors and attack itself. When this happens, autoimmune diseases can develop (e.g., lupus, rheumatoid arthritis).
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82
Q

what count as pathogens

A
bacteria
viruses
fungi
single-cell Protozoa 
multicellular parasites
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83
Q

what is an antigen

A

toxin or other foreign substance which induces a specific immune response in the body, especially the production of antibodies

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84
Q

cells involved in innate immune response

A
natural killer cells
macrophages
neutrophils
dendritic cells
mast cells
basophils
eosinophils
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85
Q

cells involved in adaptive immunity

A

T and B lymphocytes

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86
Q

what is autoimmunity

A

is the system of immune responses of an organism against its own healthy cells, tissues and other body normal constituents.

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87
Q

what is immunopathology

A

tissue damage due to excessive immune response

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88
Q

what is an allergy

A

mounting an immune response due to environmental material

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89
Q

what is immunodeficiency

A

lack of functional immune response

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90
Q

skins physical barrier description

A

multi-layered stratified squamous epithelium

dead , cornified, non -nucleated cells bound in keratin

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91
Q

describe chemical barrier of skin

secretions from sweat? secretions from sebaceous glands?

A

lacking water
secretions from sweat: lactic acid, alcohol,lysozyme
secretions from sebaceous glands: free fatty acids, wax

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92
Q

describe microbiological factor of skin

A

commensals (normal flora)
reduce nutrients and produce fatty acids
compete with pathogens

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93
Q

describe physical barrier of alimentary canal

A

peristalsis by the oesophagus

desquamation (The shedding of the outer layers of the skin. )

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94
Q

describe mucus barrier of alimentary canal

A

sticky

peristaltic waves

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95
Q

describe chemical barrier of alimentary canal

A

stomach acid (pH 2)
gastric enzymes
pancreatic enzymes
bile salts

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96
Q

urinary tract defences

A

physical barrier: resistant multi-layered epithelium
primary defence is flushing
low pH of urine
urinary stasis (cystitis)

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97
Q

vaginal epithelium defences

A

chemical/microbiological barriers
low pH during menstrual years
estrogen stimulates glucagon for normal flora

98
Q

cornea/conjunctiva defences

A

blinking

lysozyme and antibodies in tears

99
Q

two mono nucleated leukocytes

A

monocytes and macrophages

100
Q

three polymorphonucleated leukocytes

A

neutrophils
basophils
eosinophils

101
Q

describe macrophages (monocytes)

A

sentinels of danger/ infection
a large phagocytic cell found in stationary form in the tissues or as a mobile white blood cell, especially at sites of infection.

102
Q

describe neutrophils

A

most abundant of all white blood cells (70%)
important in fighting early phases of bacterial infection
amoeboid movement (most common mode of locomotion in eukaryotic cells)
diapedesis (the passage of blood cells through the intact walls of the capillaries, typically accompanying inflammation.)
chemotaxis
phagocytosis
usually self-destruct after phagocytosis 5-25 cells or bacteria
average lifespan of a few days

103
Q

what is an eosinophil

A

re a variety of white blood cells and one of the immune system components responsible for combating multicellular parasites and certain infections in vertebrates

104
Q

basic overview of interferon system

A

Interferons are proteins that are part of your natural defenses. They tell your immune system that germs or cancer cells are in your body. And they trigger killer immune cells to fight those invaders. Interferons got their name because they “interfere” with viruses and keep them from multiplying

105
Q

NK (natural killer) cells

A
Natural killer (NK) cells are effector lymphocytes of the innate immune system that control several types of tumors and microbial infections by limiting their spread and subsequent tissue damage.
very short lived 7-8 hours
recycled by liver
106
Q

what is humoral immunity

A

mediated by macromolecules (secreted antibodies, complement proteins, certain antimicrobial peptides)
located in extracellular fluid.
involves substances found in the humors (body fluids)

Humoral immunity is the process of adaptive immunity manifested by the production of antibodies by B lymphocytes. It develops in bone marrow. B cells may be triggered to proliferate into plasma cells. Plasma cells produce antibodies. Antibodies are produced when the antigen bonds the B cell receptor

107
Q

what are immunoglobulins called when they’ve been secreted

A

antibodies

108
Q

what is an antigen

A

any molecule that is recognised by, or specifically binds to, the antigen binding domain of an antigen receptor

109
Q

what are endogenous antigens

A

they are synthesised within cells and can be self or non-self (e.g. from replicating virus after infection)

110
Q

what are exogenous antigens

A

they are brought into the cell and can be self or non-self

e.g. from phagocytosis of a bacterium or a diseased cell

111
Q

what antigens can B cells and T cells recognise

A

B cells recognise any antigen

T cells limited (only short linear amino acid sequences of peptides)

112
Q

what is an antibody

A

a protein that binds specifically to a particular antigen

113
Q

how do B cells recognise antigens

A

they recognise their related antigen in its native form
B cell receptor used in recognition can also be secreted to bind to antigen and initiate multiple effector functions such as phagocytosis, complement activation or neutralisation of receptors

114
Q

basic structure of an antibody

A

Y formation made up of two light chains and two heavy chains
each light chain consists of one variable region and one constant region
each heavy chain consists of one variable region and multiple constant region domains

115
Q

Fab in structure of antibodies

A

fragment antibody binding

116
Q

fc in structure of antibodies

A

fragment crystallisable

117
Q

five different classes of immunoglobulins (antibodies)

A
IgE
IgM
IgA
IgG
IgD
118
Q

two immunoglobulin isotypes that appear as subclasses

A

IgG (IgG1, IgG2, IgG3, IgG4)

IgA (IgA1, IgA2)

119
Q

which immunoglobulin is secreted by plasma cells and released as a pentamer

A

IgM

120
Q

which immunoglobulin is secreted across mucosal surfaces

A

IgA

121
Q

properties of IgA

A

found in mucous, saliva, tears and breast milk
protects against pathogens
(Looks like a straight line?)

122
Q

properties of IgD

part of what receptor, activates what cells, what structure

A

part of the B cell receptor
activates basophils and mast cells
Y shape structure

123
Q

Properties of IgE

protects against, responsible for, what shape structure

A

protects against parasitic worms
responsible for allergic reactions
Y shape structure

124
Q

properties of IgG

A

secreted by plasma cells in the blood
able to cross the placenta into the foetus
Y shape structure

125
Q

properties of IgM

A

may be attached to the surface of the B cell or secreted into the blood
responsible for early stages of immunity
pentamer structure

126
Q

which immunoglobulin is the smallest

A

IgG (Can get everywhere)

127
Q

discuss transfer of maternal antibodies

A

immune system poorly developed at birth
mammals transfer antibodies via colostrum (the first secretion from the mammary glands after giving birth, rich in antibodies.) for the first 24-48hrs
gives protection for the first few months before production of own antibodies
IgG protects foetus

128
Q

which antibodies are responsible for neutralisation of bacteria, viruses and toxins?

A

IgA, IgG and IgM

129
Q

which antibodies are responsible for opsonisation ? describe it

A

IgA and IgG
antibody-coated bacterium binds to Fc receptors on cell surface
macrophage membrane surrounds bacterium
macrophage membrane fuses creating a membrane-bound vesicle , the phagosome

130
Q

What is ADCC

A

antibody dependent cellular cytotoxicity

131
Q

what antibody is responsible for ADCC - describe it

A

IgG
antibody binds antigens on the surface of target cells
Fc receptors on NK cells recognise bound antibody
cross linking of Fc receptors signals the NK cells to kill the target cells
target cell dies by apoptosis and/or membrane damage

(ADCC is A type of immune reaction in which a target cell or microbe is coated with antibodies and killed by certain types of white blood cells. )

132
Q

describe activation of complement cascade by IgG

A

IgG molecules bind to antigens on bacterial surface
C1q binds to at least two IgG molecules

(the complement component 1q is a protein complex involved in the complement system, which is part of the innate immune system. C1q together with C1r and C1s form the C1 complex. Antibodies of the adaptive immune system can bind antigen, forming an antigen-antibody complex. )

133
Q

Describe activation of complement cascade by IgM

A

pentameric IgM molecules binds to antigens on bacterial surfaces and adopt ‘staple’ form
C1q binds to IgM

(the complement component 1q is a protein complex involved in the complement system, which is part of the innate immune system. C1q together with C1r and C1s form the C1 complex. Antibodies of the adaptive immune system can bind antigen, forming an antigen-antibody complex. )

134
Q

which antibody trigger mast cell activation

A

IgE

135
Q

which antibody triggers eosinophil activation (Describe)

A

IgE

helps to destroy multi-cellular parasites

136
Q

describe isotope switching after activation (antibodies)

A

all newly formed B cells express monomeric IgM and IgDat the cell surface as receptors
following activation B cells undergo isotope switching in order to produce different types of antibodies

137
Q

what is the primary immune response characterised by (think graph)

A
  • lag phase - during which B cells undergo clonal selection in response to antigen, proliferate and differentiate into plasma cells or memory cells (typically 4-7 days)
  • then an exponential increase in serum antibody levels
  • peak in antibody level at 7-10 days followed by a decline in antibody levels
  • initially all IgM secretion but some IgG produced late in the primary response
  • formation of memory B cells
138
Q

what does clonal expansions and B cell memory mean

A

that the immune response gets bigger on each encounter

139
Q

what does isotype switching mean (in terms of antibodies)

A

initially IgM dominates the response, but that this is replaced by IgG

140
Q

what does somatic mutation mean (in terms of antibodies)

A

definition: somatic mutation is a change in the DNA sequence of a somatic cell of a multicellular organism with dedicated reproductive cells; that is, any mutation that occurs in a cell other than a gamete, germ cell, or gametocyte

means that as the response develops the affinity of the antibody increases

141
Q

what is the secondary immune response characterised by

A
  • mediated by memory B cells formed in the primary immune response
  • shorter lag phase than primary
  • more antibody production than primary
  • antibody is of higher affinity for antigen than in the primary (called affinity maturation)
  • includes various isotopes in addition to IgM
142
Q

define plasma cells

A

A type of immune cell that makes large amounts of a specific antibody. Plasma cells develop from B cells that have been activated. A plasma cell is a type of white blood cell. Also called plasmacyte

143
Q

what are lymphocytes

A

clones

144
Q

describe t cells

A

produced in bone marrow

mature in thymus before entering the circulation

145
Q

what are dendritic cells

A

professional antigen presenting cells (APCs) that present antigens to T cells
(take up fragments of microbes in inflamed tissue and then take them to the local lymph nodes too show them to T and b cells

146
Q

describe when an APC and T cell come together

A

the membrane connecting them is folded
tcr( T cell receptor) does not bind to soluble antigen
it recognises peptide fragments of antigens presented by MHC molecules

147
Q

MHC molecules??

A

major histocompatibility complex

gene complex that codes for the molecules

148
Q

cells that present MHC class I

A

all nucleated cells except
neurones
sperm cells
certain cells within placenta

149
Q

cells that present MHC class II

A

APCs: (Antigen presenting cells)
dendritic cells
B cells
macrophages

150
Q

3 different types of T cells

A

Th1 - t helper 1
Th2 - t helper 2
CTL - T cytotoxic

151
Q

Describe TH1 (co receptor, antigen source and MHC binding class)

A

co receptor - CD4
antigen source - exogenous (synthesis outside)
MHC binding class II

152
Q

Describe TH2

co receptor, antigen source and MHC binding class

A

Co receptor CD4
antigen source - exogenous (synthesis outside)
MHC binding class II

153
Q
Describe CTL
(co receptor is, antigen source is, MHC binding class)
A

Cytotoxic T-lymphocyte.

Co receptor CD8
antigen source endogenous (synthesis within)
MHC binding class I
154
Q

describe endogenous antigen MHC class I

A

MHC class I molecules (MHC-I) are cell surface recognition elements expressed on virtually all somatic cells. These molecules sample peptides generated within the cell and signal the cell’s physiological state to effector cells of the immune system, both T lymphocytes and natural killer (NK) cells.

  • cell infected by virus or bacteria or cancer cell
  • newly made foreign / self proteins expressed within cytoplasm
  • proteins ubiquitinated (form of post-translational modification in which the ubiquitin-protein is attached to a substrate protein) and broken downing peptide by proteosome
  • peptides transported via to ER, complexed with MHC class I proteins , inserted into membrane
  • recognised by CD8+ cytotoxic T cells
  • activation of killer T Cells
155
Q

describe exogenous antigen MHC Class II

A

The main function of major histocompatibility complex (MHC) class II molecules is to present processed antigens, which are derived primarily from exogenous sources, to CD4(+) T-lymphocytes. MHC class II molecules thereby are critical for the initiation of the antigen-specific immune response.

-extracellular antigens
- taken up by endocytosis by APCs
- degraded into peptides in a phagosome
-phagosomes fuse with MHC class II containing vesicles , complex with peptides, inserted into membrane
-recognised by CD4+ helper T cells
_activation of helper T cells

156
Q

what do TH1 help fight against

A

intracellular bacteria
viruses
cancer

157
Q

what do TH2 help fight against

A

extracellular bacteria
parasites
toxins
allergens

158
Q

`what do cytokines do

A

alter behaviour of target cells

159
Q

what do cytotoxins do

A

kill the target cell (by apoptosis)

160
Q

impact of viral diseases on society

A

pandemics, epidemics etc
directed health impact - acute and chronic illness , death
indirect - loss of function(not working), loss of earnings, economic productivity, healthcare costs

161
Q

UK viral emergencies

A

viral haemorrhagic fevers
rabies
MERS CoV
avian influenza A (Bird flu)

162
Q

what is a virus particle ( virion) composed of

A

virus genome (nucleic acid) - DNA or RNA but not both
protein capsid (coat)
may possess an envelope
may include replicative enzymes

163
Q

four principle criteria for classification of virus

A

nature of nucleic acid in virion (virus particle)
symmetry of capsid
presence or absence of envelope
dimensions of virion and capsid

164
Q

typical lifecycle of enveloped virus

A
attachment 
penetration - fusion or endocytosis
uncoating
genome replication - and gene expression
assembly
maturation
release
165
Q

what is viral pathogenesis

A

process by which viral infection leads to disease

virus doesn’t want to harm host - its our immune system that hurts us

166
Q

factors in viral pathogenesis

A
  • portal of entry and course of infection (primary replication, systemic spread, secondary replication)
  • cell/tissue tropism (the ability of a given virus to productively infect a particular cell (cellular tropism), tissue (tissue tropism) or host species (host tropism)
  • cell/tissue damage - direct and indirect (lysis, host immune response)
167
Q

virus and host factors that determine outcome of infection

A

virulent virus strain causes significant disease
avirulent or attenuated strain causes no or reduced disease
host factors - age, gender, immunity, immunosuppression, genetic susceptibility

168
Q

types of transmission

A

direct - contact, droplets, aerosol
indirect - vehicle borne, fomites (objects or materials which are likely to carry infection, such as clothes, utensils, and furniture), vectors, airborne
resp. secretions, urine, vomit, blood, semen

169
Q

two main mechanisms for intra-host viral spread

A

via blood stream and lymphatic system

via nervous system

170
Q

define viraemia

A

presence of virus in the blood

171
Q

what’s lymphadenopathy or adenopathy

A

disease of the lymph nodes where they are abnormal in size or consistency

172
Q

what is viral tropism determined by

A

presence of cellular receptors
cellular proteins that regulate viral replication
cellular proteins that regulate viral transcription
cellular proteins which “activate” viruses
accessibility of susceptible cells

173
Q

describe primary infection of herpes simplex virus

A

usually colds sores
sore throat
fever
rarely - encephalitis (inflammation of the brain)

174
Q

describe the latent infection of herpes simplex

A

asymptomatic - no virus produced

viral DNA resides in sensory cells of trigeminal nerve ganglion

175
Q

describe the reactivation phase of herpes simplex

A

virus replicates and travels down sensory nerve fibre to infect epithelial cells around the nose and mouth

176
Q

Basic concept of vaccination

A

Vaccination: The act of introducing a vaccine into the body to produce protection from a specific disease. Immunization: A process by which a person becomes protected against a disease through vaccination. This term is often used interchangeably with vaccination or inoculation.

177
Q

what is meant by herd immunity

A

form of indirect protection from infectious disease that can occur with some diseases when a sufficient percentage of a population has become immune to an infection, whether through previous infections or vaccination, thereby reducing the likelihood of infection for individuals who lack immunity

178
Q

what is a live vaccine

A

made from a virus that has been weakened so it does not cause the disease the virus usually causes. A live virus vaccine helps the body’s immune system recognize and fight infections caused by the non-weakened form of the virus.

179
Q

what is an attenuated vaccine

A

vaccine created by reducing the virulence of a pathogen, but still keeping it viable. Attenuation takes an infectious agent and alters it so that it becomes harmless or less virulent. These vaccines contrast to those produced by “killing” the virus.

180
Q

what is a subunit vaccine

A

A subunit vaccine is a vaccine that contains purified parts of the pathogen that are antigenic, or necessary to elicit a protective immune response.

181
Q

define bacteria

A

a member of a large group of unicellular microorganisms which have cell walls but lack organelles and an organized nucleus, including some that can cause disease.

182
Q

define virus

A

.
an infective agent that typically consists of a nucleic acid molecule in a protein coat, is too small to be seen by light microscopy, and is able to multiply only within the living cells of a host

183
Q

define eukaryote

A

an organism consisting of a cell or cells in which the genetic material is DNA in the form of chromosomes contained within a distinct nucleus. Eukaryotes include all living organisms other than the eubacteria and archaea.

184
Q

define parasite

A

an organism that lives in or on an organism of another species (its host) and benefits by deriving nutrients at the other’s expense

185
Q

define prion

A

Prions are misfolded proteins with the ability to transmit their misfolded shape onto normal variants of the same protein. They characterize several fatal and transmissible neurodegenerative diseases in humans and many other animals.

186
Q

define infection

A

The invasion and growth of germs in the body. The germs may be bacteria, viruses, yeast, fungi, or other microorganisms. Infections can begin anywhere in the body and may spread all through it. An infection can cause fever and other health problems, depending on where it occurs in the body.

187
Q

define contagious

A

spread from one person or organism to another, typically by direct contact.

188
Q

define comensal pathogen

A

Living in a relationship in which one organism derives food or other benefits from another organism without hurting or helping it. Commensal bacteria are part of the normal flora in the mouth.

189
Q

define virulence

A

is a pathogen’s or microorganism’s ability to cause damage to a host

190
Q

define microbiome

A

the microorganisms in a particular environment (including the body or a part of the body).

191
Q

Difference in structure between eukaryotic and prokaryotic cells

A

include the presence of mitochondria and chloroplasts, the cell wall, and the structure of chromosomal DNA.

192
Q

risks of antimicrobial use

A

Increased antimicrobial resistance is the cause of severe infections, complications, longer hospital stays and increased mortality. Overprescribing of antibiotics is associated with an increased risk of adverse effects, more frequent re-attendance and increased medicalization of self-limiting conditions.

193
Q

what is a coccus

A

any spherical or roughly spherical bacterium.

194
Q

what is a bacilli

A

bacillus, or bacilliform bacterium, is a rod-shaped bacterium or archaeon.

195
Q

what is a vibrios

A

water-borne bacterium of a group that includes some pathogenic kinds that cause cholera, gastroenteritis, and septicaemia.
curved rod-shape

196
Q

what is a spirochetes

A

a flexible spirally twisted bacterium, especially one that causes syphilis.

197
Q

what is colonisation

A

colonization is the presence of bacteria on a body surface (like on the skin, mouth, intestines or airway) without causing disease in the person

198
Q

what is contamination

A

the presence of a constituent, impurity, or some other undesirable element that spoils, corrupts, infects, makes unfit, or makes inferior a material, physical body, natural environment, workplace, etc

199
Q

difference between endo and ectoparasites

A

Endoparasites live inside an organism, and ectoparasites live on the surface of the host. Parasites can be carnivorous if living with animals or herbivorous if living with plants.

200
Q

define incubation period

A

Incubation period is the time elapsed between exposure to a pathogenic organism, a chemical, or radiation, and when symptoms and signs are first apparent

201
Q

define infectious period

A

is the time interval during which a host is infectious, i.e. capable of directly or indirectly transmitting pathogenic infectious agents or pathogens to another susceptible host

202
Q

define transmissibility

A

the quality of a disease or trait being able to be passed on from one person or organism to another.

203
Q

how does Clostridium tetani form endopsores that resist extremes of temperature

A

The cortex is what makes the endospore so resistant to temperature. The cortex contains an inner membrane known as the core. The inner membrane that surrounds this core leads to the endospore’s resistance against UV light and harsh chemicals that would normally destroy microbes.

204
Q

transmission of meningococcus

A

people spread meningococcal bacteria to other people by sharing respiratory and throat secretions (saliva or spit).

205
Q

explain term sepsis

A

the body’s extreme response to an infection. It is a life-threatening medical emergency. Sepsis happens when an infection you already have triggers a chain reaction throughout your body. Infections that lead to sepsis most often start in the lung, urinary tract, skin, or gastrointestinal tract.

206
Q

basic principle of gram staining

A

involves the ability of the bacterial cell wall to retain the crystal violet dye during solvent treatment.

207
Q

what does hypersensitivity mean

A

describes an adverse reaction to an antigen

208
Q

Four types of hypersensitivity

A

Type I - IgE mediated
type II - IgG mediated
Type III - immune complex mediated
Type IV- T cell mediated

209
Q

Factors affecting Th1 phenotype

A

presence of older siblings
early exposure to day care
TB, measles, or hepatitis A infection
rural environment

210
Q

Factors affecting Th2 phenotype

A
widespread use of antibiotics
western lifestyle
urban environment 
diet
sensitisation to house dust mites and cockroaches
211
Q

Describe initiating event of Type I hypersensitivity

A
IgE dependent
soluble antigen (allergen)
triggers IgE response
subsequent antigen exposure leads to interaction with IgE on mast cells 
IgE bound by FcRe
mast cell/basophil degranulation

example of this response is anaphylaxis

212
Q

what is type II hypersensitivity divided into

A

IIa - cytotoxic

IIb- cell stimulating/signalling

213
Q

Type IIa hypersensitivity

A

IgG antibody interacting with cell surface antigen
antigen cell associated
may be happen (a small molecule which, when combined with a larger carrier such as a protein, can elicit the production of antibodies which bind specifically to it (in the free or combined state).) interaction
binding of IgG leads to lysis of target cells
complement mediated

214
Q

type IIb hypersensitivity

what immunoglobulin mediated?

A

cell stimulating reactions involving altered cell function
IgG mediated
IgG interacts with cell surface receptor involved in cell signalling
antigen cell associated

215
Q

Type III hypersensitivity

A
antigen - antibody complexes (IgG)
antigen soluble or matrix associated
deposit in microvasculature
complement activation
tissue inflammation
216
Q

Type IV hypersensitivity divided into

A

Th1
Th2
cytotoxic
Ivd

217
Q

Type IV Th1 hypersensitivity

A
classical delayed type hypersensitivity
antigen presentation to sensitised CD4 Th1 cells 
soluble antigen
Th1 cytokine production and release
macrophage activation
macrophage rich antibody response

contact dermatitis
drug allergies

218
Q

TypeIV th2 hypersensitivity

A

cell-mediated eosinophilic hypersensitivity (chronic allergic inflammation)
antigen presented to sensitised predominately CD4 Th2 cells
soluble antigen
eosinophil rich inflammatory response

219
Q

examples of Type IV th2 hypersensitivity

A

chronic asthma
chronic allergic rhinitis
topic eczema

220
Q

Type IV cytotoxic hypersensitivity

A

antigen presented to sensitised CD8 T cells
antigen cell associated
cytotoxicity - perforin

221
Q

examples of Type IV cytotoxic hypersensitivity

A

early onset type 1 diabetes mellitus
graft rejection
some drug reactions

222
Q

describe autoimmune disease

A

adaptive immune system recognises self antigen as harmful and amounts an immune attack

223
Q

describe auto-inflammatory disease

A

results from over activity of the innate system
may be activated by triggers but genetic mutations can cause triggers

Innate: from when you were born

224
Q

what happens in auto-inflammatory disease

A

raised inflammatory markers

absence of infection

225
Q

what is iatrogenic anaphylaxis

A

drug induced anaphylaxis

226
Q

organism for common cold, pneumonia, influenza

A

cold - rhinovirus
pneumonia - Streptococcus pneumoniae
influenza - Orthomyxovirus genus.

227
Q

transmission of common cold, pneumonia, influenza

A

cold- air, close contact, contact with stool, respiratory secretions
pneumonia - cough, sneezes, respiratory secretions
influenza - droplets

228
Q

how to distinguish between influenza and pnuemonia

A

The flu usually comes on suddenly, while pneumonia takes longer to develop and can be a complication from the flu.

229
Q

is IgE found in early infection

A

no

230
Q

In an indirect ELISA is the enzyme is linked to a secondary antibody?

A

yes

231
Q

5mg/ml is diluted 5 fold 3 times

A

0.04

232
Q

Cell surface markers present on t helper cells

A

TcR

CD4

233
Q

What is the single most important requirement for samples to be analyzed on a flow cytometer?

A

cells must be in single cell suspension

234
Q

role of disinfectants in killing bacteria

A

They kill off the bacteria by causing the proteins to become damaged and the outer layers of the bacteria cell to rupture. The DNA material subsequently leaks out.

235
Q

does toilet paper act as an effective barrier to bacterial transmission

A

no

236
Q

Direct ELISA

A

○ Uses monoclonal antibodies to detect presence of particular antigen in a sample
○ Can be used to measure amount of antigen labelled primary antibody
§ In this case antigen is usually bound to the well of an ELISA plate
§ After labelled antibody binds to the antigen it can be detected through an enzyme reaction

237
Q

Indirect ELISA

A

○ Used to determine presence of specific antibody (eg. Antibodies to HIV) in a specimen such as serum
○ Involves at least two different antibodies
§ Primary antibody will be specific for antigen of interest but is not linked to an enzyme
§ Secondary antibody specific for primaru antibody will be conjugated (covalently linked) to an enzyme and it is therefore possible to quantify how much primary antibody has bound to the antigen of interest

238
Q

Capture ELISA

A

○ Capture ELISA or ‘sandwich’ ELISA variation on the indirect method
§ Allows complex antigen samples (such as serum) to be analysed for presence of specific antigen or the presence of an antibody against a specific infection

239
Q

analysing ELISA plates

A
  • Antibody specific to virus antigen will bind to the antigen and any unbound antibody is washed away
    • Second reaction is performed where anti-human immunoglobulin that is coupled to an enzyme (enzyme-linked antibody) is added and binds to primary antibody and any unbound antibody is washed away
    • Substrate is then added and enzyme acts off this substrate causing a colour change, the stronger the antibody response the stronger the colour
    • Plate is ‘read’ in a plate reader using light with a wavelength of 405nm and the detector will report the absorbance of light as a numerical (optical density) OD405 reading
240
Q

flow cytometry

A

technology that rapidly analyzes single cells or particles as they flow past single or multiple lasers while suspended in a buffered salt-based solution. Each particle is analyzed for visible light scatter and one or multiple fluorescence parameters. … Light scatter is independent of fluorescence.

241
Q

what does perforin do

A

causes pores to form in target cells membrane

242
Q

what do granzymes do

A

enter cell and induce apoptosis seen as DNA fragmentation