Pathophys - Immunity & Inflammation

Front 1

define the immune response

Back 1

a collective and coordinated response of cells of the immune system

Front 2

define the immune response

Back 2

a collective and coordinated response of cells of the immune system

Front 3

3 functions of the immune sys

Back 3

1. protect host f/foreign invasion (bacteria, parasites, etc)
2. distinguishes self f/non self (ca, autoimmune rxn, blood/organ transplant)
3. mediates healing (modulates inflammatory process and wound repair)

Front 4

dysfunction leads to 4 things

Back 4

1. immunodeficiency
2. allergies/hypersensitivities
3. transplantation pathology
4. autoimmunity

Front 5

3 functions of the immune sys

Back 5

1. protect host f/foreign invasion (bacteria, parasites, etc)
2. distinguishes self f/non self (ca, autoimmune rxn, blood/organ transplant)
3. mediates healing (modulates inflammatory process and wound repair)

Front 6

define innate immunity

Back 6

-natural resistance person is born with
-comprises physical, chemical, and cellular barriers
- first line of defense
ex: skin, mucous membranes, tears

Front 7

dysfunction leads to 4 things

Back 7

1. immunodeficiency
2. allergies/hypersensitivities
3. transplantation pathology
4. autoimmunity

Front 8

define adaptive immunity

Back 8

-acquired
-specific
-amplified response with memory
- 2 components:
-cell mediated
- antibody mediated (humoral)

Front 9

define innate immunity

Back 9

-natural resistance person is born with
-comprises physical, chemical, and cellular barriers
- first line of defense
ex: skin, mucous membranes, tears

Front 10

define adaptive immunity

Back 10

-acquired
-specific
-amplified response with memory
- 2 components:
-cell mediated
- antibody mediated (humoral)

Front 11

antibody mediated immunity if triggered by encounters with:

Back 11

antigens

Front 12

antibodies are also known as:

Back 12

immunoglobulins

Front 13

innate immunity is driven by:

Back 13

cells (monocytes, macrophages, dendritic cells, neutrophils, eosinophils)

Front 14

monocytes are in the ______
macrophages are in the ______

Back 14

blood
tissues

Front 15

monocytes, macrophages, and dendritic cells are all:

Back 15

phagocytes

Front 16

neutrophils are also called

Back 16

polymorphonuclear leukocytes

Front 17

neutrophils' role in inflammatory response

Back 17

first line defender against bacterial invasion, colonization and infectio

Front 18

eosinophils are part of the:

Back 18

inflammatory response

Front 19

what do eosinophils fight?

Back 19

parasites, esp worms

Front 20

eosinophils may release chemicals in the resp tract r/t what disease process?

Back 20

allergies, asthma

Front 21

when activated, monocytes, macrophages, and dendritic cells phagocytize things and release ______

Back 21

cytokines

Front 22

neutrophils are great at:

Back 22

antigen binding and non-specific phagosytosis

Front 23

basophils release mediators (es: histamine) during what type of responses?

Back 23

allergic responses

Front 24

basophils have binding sites for:

Back 24

IgE (type 1 hypersensitivity)

Front 25

basophils reside in:

Back 25

the blood

Front 26

mast cells are located in:

Back 26

the tissue

Front 27

mast cells release:

Back 27

histamine

Front 28

histamine is

Back 28

the hallmark of tissue inflammatory response

Front 29

natural killer cells are:

Back 29

effector cells, important in innate immunity

Front 30

a small number of lymphocytes become:

Back 30

natural killer cells

Front 31

without help or activation, a natural killer cell can:

Back 31

attack virus infected or cancer cells

Front 32

natural killer cells can bind with:

Back 32

an antibody coated target cell (antibody dependent cell mediated cytotoxicity (ADCC))

Front 33

natural killer cells can recognize an antigen:

Back 33

without MHC restrictions. they have NO MEMORY

Front 34

natural killer cells are regulated by:

Back 34

cytokines, protaglandins, thromboxane

Front 35

cytokines are:

Back 35

small, low MW, hormone like proteins, produced during all phases of the immune response

Front 36

cytokines are made by:

Back 36

T cells and macrophages

Front 37

cytokines primarily act on:

Back 37

immune cells

Front 38

cytokines are involved in:

Back 38

innate immunity, adaptive immunity, hematopoiesis

Front 39

define inflammation

Back 39

reaction of vascularized tissue to local injury (cellular) manifesting as redness, swelling, heat, pain, loss of function

Front 40

is inflammation specific or non specific?

Back 40

non specific - chain of events is similar regardless of injury type and extent

Front 41

what triggers inflammation?

Back 41

breaching of the body's first line fo defense (skin, mucous membrane) - must reach vascularized tissue

Front 42

inflammation can have this side effect:

Back 42

inflammatory disease

Front 43

describe phase 1 of the acute inflammation response:

Back 43

1. Vascular Phase: rapid vasoconstriction, rapid vasodilation (erythema & warmth), increasing capillary permeability

Front 44

depending on the severity of injury, 3 inflammation scenarios are possible:

Back 44

1. immediate transient response (minor injury)
2. immediate sustained response (several days, causes damaged vessels)
3. delayed hemodynamic response (sunburn, etc -f/the inside out)

Front 45

describe phase 2 of the acute inflammation response:

Back 45

2. cellular phase - phagocytes move to site of injury & release cytokines, chemotaxis begins, increasing cap perm allows leukocytes to migrate to injury

Front 46

what does histamine do?

Back 46

one of the first mediators of inflammation, it causes dilation and increased cap perm

Front 47

there is a high concentration of histamine in:

Back 47

platelets, basophils, mast cells

Front 48

in mast cells, histamine is released in response to binding of:

Back 48

IgE antibodies

Front 49

bradykinin (a plasma protease) causes:

Back 49

increased cap perm and pain

Front 50

arachidonic acid is:

Back 50

a signalling protein in the cell membrane

Front 51

arachidonic acid is metabolized into:

Back 51

prosteglandins or leukotrienes

Front 52

arachidonic acid is metabolized into prosteglandins via the:

Back 52

cyclooxygenase pathway

Front 53

arachidonic acid is metabolized into leukotrienes via the:

Back 53

lipoxygenase pathway

Front 54

platelet activating factor (an inflammatory mediator) does what?

Back 54

induces platelet aggregation, neutrophil activation, and eosinophil chemotaxis

Front 55

the complement system is:

Back 55

a nebulous circulating system, a primary mediator of the innate and adaptive humoral immune response

Front 56

the complement system can produce:

Back 56

inflammatory response, lysis of foreign cells, increasing phagocytosis

Front 57

is the complement system specific or non specific?

Back 57

non specific, no memory

Front 58

name the 3 independent (yet parallel) pathways to complement system activation:

Back 58

Classical Pathway: 1. binding of IgG or IgM to invading organisms 2. binding of complement to circulating antigen/antibody complex (complement fixation)

Alternate Pathway: triggered by interactions b/t complement and polysaccharides on microbes

Lectin Pathway: activated by binding proteins interacting with cell surface proteins in bacteria and yeast

*all pathways converge to a common point

Front 59

when activation pathways of complement converge, what happens?

Back 59

-MAC insertion into target cell membrane
-opsonization (coating) AgAb complexes to help neutrophils and macrophages phagocytize
-stimulates mast cells and basophils to release histamine to attract neutrophils & others
- anaphylatoxin produced, which causes histamine release, contraction of smooth musc, increased vasc perm, edema

(MAC, opsonization, chemotaxis, anaphylatoxin)

Front 60

chronic inflammation is caused by:

Back 60

low grade persistent irritants (talk, silica, asbestos, surgical sutures, some bacteria (TB, syphilis), injured tissue around a fracture)

Front 61

2 patterns of chronic inflammation

Back 61

1. non specific diffuse accumulation of macrophage \s & lymphocytes, leading to fibroblasts & scar tissue
2. granuloma (splinters, TB tubercule)

Front 62

2 causes of chronic inflammation

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1. recurrent/progressive acute inflammation
2. low grade responses that fail to evoke acute responses

Front 63

characteristics of acute inflammation:

Back 63

- infiltration by mononuclear cells (macs & lymphs) NOT neutrophils like in acute
- proliferation of fibroblasts = scarring; not exudates

Front 64

why is exudate a local manifestation of inflammation?

Back 64

- extravascular influx of fluid
- fluid dilutes injurious chemicals
- fluid brings in complement, Abs, & other chemotactic substances d/t osmotic gradient
- extra vascular proteins pull water out of the plasma

Front 65

describe serous exudate

Back 65

watery, low in protein

Front 66

fibrinous

Back 66

large amts of fibrinogen. slick, lubricating.

Front 67

membranous

Back 67

necrotic debris in fibrinous matrix on mucus membrane surfaces

Front 68

purulent

Back 68

degraded white cells, protein, tissue debris

Front 69

hemorrhagic

Back 69

severe leakage of red cells f/capillaries

Front 70

local inflammation becomes systemic when:

Back 70

the site of inflammation is large enough or robust enough to induce systemic response (fever, leukocytosis, skeletal musc catabolism)

Front 71

most inflammatory mediators have a short half life, so:

Back 71

autocrine and paracrine signalling predominates

Front 72

systemic inflammation - acute manifestations

Back 72

-increase in plasma proteins
- increased ESR
- fever
- leukocytosis (presence of immature neutrophils "bands")
- skeletal muscle catabolism (mobilize aa f/protein synthesis)
- negative nitrogen balance
- lympadenitis

Front 73

adaptive immunity - 2 types of active

Back 73

1. immunizations
2. having the disease
(your body is actually exposed to the disease and responds - it stores it in the memory)

Front 74

adaptive immunity - type of passive

Back 74

- transferred f/another source (in utero, breast milk, antibody infusion)
- short term - your body does not make it, so it does not remember it

Front 75

5 characteristics of the adaptive immune response:

Back 75

1. self tolerance - self vs non
2. self regulation - can initiate, maintain, down regulate, without help
3. specificity - targets specific antigens
4. diversity - invokes a specific response depending on Ag
5. memory - makes memory cells (only IS and CNS)

Front 76

B cell lymphocytes (2):

Back 76

1. plasma B cells
2. memory B cells

Front 77

T cell lymphocytes (2):

Back 77

1. T helper cells
2. Cytotoxic T cells

Front 78

Antigens (aka immunogens) are:

Back 78

- foreign to host
- stimulate an immune resp
- are recognized by receptors on immune cells & antibodies (Igs)
- are ofter proteins or polysaccharides, less often lipids or nucleic acids

Front 79

Antigens are found on:

Back 79

bacteria, fungi, protozoa, parasites, non-microbial agents such as pollen, plant resin, venom, tx organ

Front 80

how do antigens stimulate an adaptive immune response?

Back 80

- lg antigens have small, immunologically active sites (epitopes)
- specific Ig receptors recognize the epitopes
- haptens are too small to stimulate an immune response unless they are bound to a protein

Front 81

Major Histocompatibility Complex (MHC) - what is it?

Back 81

-cell surface molecules which provide a mechanism to differentiate self f/non self
- region of genetic info that makes each individual different (even in the same species)
- human leukocyte antigens (HLA) were the first identified on WBCs

Front 82

what recognizes MHC?

Back 82

cytotoxic T and helper T

Front 83

MHC II are found on:

Back 83

antigen presenting cells, such as macrophages, dendritic cells, b lymphocytes. helper Ts recognize antigens stuck on the MHC II

Front 84

MHC I are on:

Back 84

every nucleated cell

Front 85

cytotoxic t cells become activated when they are presented with:

Back 85

an antigen associated with a class I MHC. the Tc kills it.

Front 86

lymphocyte stem cells are in the:

Back 86

bone marrow

Front 87

lymphocytes which migrate thru lymphoid tissue become:

Back 87

B cells (make antibodies)

Front 88

lymphocytes which migrate thru the thymus become:

Back 88

T cells (cell-mediators)

Front 89

B lymphocytes are responsible for:

Back 89

antibody production (humoral immunity)

Front 90

what is the function of a B lymphocyte?

Back 90

- act as a receptor to a specific antibody
- manufacture specific antibodies to target one specific antigen
- only recognize one antigen

Front 91

After mature B lymphocytes leave the bone marrow, they enter the blood and travel to the tissue. Then what?

Back 91

with the help of a Th, they bind an antigen and differentiate into plasma cells (lg #, responsible f/antibody secretion) and memory cells (sm #)

Front 92

B lymphocytes secrete antibodies (humoral immunity). Primary immune response is:

Back 92

-antigen enters body and is processed by antigen presenting cells
- MHC complexed antigen is recognized by Th cells
- Th cells release cytokines & trigger B lymphocytes to proliferate (plasma & memory)
- plasma cells release antibody
-this takes a while!

Front 93

what % of SNRAs taking pathophys wish they had already taken it?

Back 93

100%

Front 94

B lymphocytes secrete antibodies (humoral immunity!). Secondary immune response is:

Back 94

-once rechallenged with antigen at a later time, the memory cells recognize it & respond quickly
- immunization boosters (eg, tetanus) take advantage of this

Front 95

antibodies (immunoglobulins) are produced by:

Back 95

B lymphocytes

Front 96

IgA

Back 96

secretory (saliva, colustrum, bronchial, pancreatic, GI, prostatic, vaginal). prevents viral and bacterial binding to epithelial tissues. THE FIRST LINE OF DEFENSE IN MUCOSAL TISSUES.

Front 97

IgM

Back 97

lg, macromolecule complex. first Ig made in response to an antigen. FIRST ANTIBODY TYPE MADE BY A NEWBORN.

Front 98

IgD

Back 98

primarily on cell membranes of B lymphocytes. acts an antigen receptor.

Front 99

IgE

Back 99

involved in inflammation, allergic response, combating parasitic infections. antigen binding to IgE on mast cells or basophils causes histamine release; important in inflammation and allergies.

Front 100

IgG

Back 100

most abundant circulating antibody in blood and the only Ab that can cross the placenta. Ig in fetus/newborn is passed f/mother until new Igs are formed by newborn. targets bacteria, virus, toxins. can activate complement.

Front 101

T lymphocytes are responsible for:

Back 101

cell mediated immunity

Front 102

T lymphocytes are formed by:

Back 102

bone marrow stem cells which migrate to the thymus for maturation. mature t cells then migrate to peripheral lympoid organs

Front 103

T lymphocytes are responsible for:

Back 103

cell mediated immunity

Front 104

T lymphocytes are formed in:

Back 104

bone marrow (stem cells), then to the thymus f/maturation. Mature T cells then migrate to peripheral lymphoid organs.