2. Inflammation

Front 1

5 cardinal signs of inflammation and explaination

Back 1

1. heat/hot: ↑ blood flow in affected area

2. redness

3. swell: ↑ bulk (gel-like)

4. pain: ↑ tension tissue

5. loss of function

Front 2

healthy, physiological outcomes of inflammation

Back 2

-can be a defense mechanism

-evolutionary term, inflammation is a protective system

Front 3

How can inflammation can be harmful

Back 3

-life threatening: fill up of air spaces in lung

-mechanical trauma: cutting/crushing

-chemical injuries: produced by acid

Front 4

Acute inflammation

Back 4

-onset: fast

-cells: neutrophils

-tissue: limited

-physical sign: obvious

Front 5

Chronic inflammation

Back 5

-onset: slow

-cells: macrophages & lymphs

-tissue: progessive

-physical sign: subtle

Front 6

2 main components of inflammation:

Back 6

1. cellular: (leukocytes) accumulation of leukocytes at site of injury (migration)

2. vascular: vasodiliation, ↑ vascular permeability

Front 7

Exudate

Back 7

↑ vascular permeability

-mass of cell & fluid that has speed out of blood vessels or organs especially in inflammation

Front 8

Transudate

Back 8

↑ hydrostatic pressure

↓ colloid osmotic pressure

Front 9

6 types of exudate:

Back 9

1. serous exudate

2. fibrinous exudate

3. haemorrhagic

4. purulent

5. catarrhal

6. membrane & pseudomembranous

Front 10

serous exudate

Back 10

↓ in protein

fluid in blister

Front 11

fibrinous exudate

Back 11

↓ volume & ↑ protein,

-two surface covered in fibrin stick together to build bridge = scar tissue form = loss of function

Front 12

Haemorrhagic exudate

Back 12

occur where small blood vessel severely damage that allow the escape of red cells from lumen into extravascular space.

Front 13

Purulent exudate

Back 13

-neutrophil dominant

-large # cells

-liquefaction of dead tissue (fluid material pus)

Front 14

Catarrhal exudate

Back 14

occur when mucous membrane is inflammed

Front 15

Membrane/Pseudomembranous exudate

Back 15

consist dead epithelial cells (fibrin+neutrophils)

Front 16

Major cells in inflammation

Back 16

white cells, endothelial cells, neutrophils, eosinophils, basophils (mast cells)

Front 17

mast cells release

Back 17

histamine

Front 18

which cells control adhesion/migration of inflammation cells

Back 18

endothelial cells

Front 19

neutrophils

Back 19

most # of cells that migrate to injured area in early stages of acute inflammation

Front 20

eosinphils

Back 20

-promote inflammation

-benefical when isolating/controlling disease site and ongoing inflammation

Front 21

basophils

Back 21

release histamine, chemotactics factors, cytokins

Front 22

Explain leukocyte recruitment (out of blood vessels into inflamed)

Back 22

1. injured/inflammed tissue

2. release chemicals

3. endothelial cells produce adhesion mol. in response to chemicals

4. white cells moving in blood

5. tether/roll

6. adhere

7. immune cell exit the blood vessel

Front 23

Leukocyte

Back 23

white blood cells that fight of bacteria

Front 24

3 steps in phagocytosis

Back 24

1. opsonization

2. engulfment

3. lysosomal fusion°ranulation

Front 25

Opsonization

Back 25

-coat microbes & target them for opsonins

-the microbes bind to phagocyte receptor

- two proteins: IgG & C3b

Front 26

Egulfment

Back 26

phagocyte membrane zips up around microbe

Front 27

Lysosomal fusion & degranulation

Back 27

break down

Front 28

phagocytosis

Back 28

it keeps bacteria foreign bodies away from other parts of cell and packs it up then kill it

Front 29

Vasoactive amines

Back 29

-histamine

-serotonin

Front 30

Histamine:

Back 30

-↑ vascular premeability = swelling

-↑ inflammatory responses

-hot, red, swollen = cause small blood vessels in -tissue to expand/dilate/leak

-allow protective blood proteins + WBCs to leave vessels & start repair.

Front 31

Serotonin:

Back 31

↑ blood pressure = constriction blood vessels (vasoconstriction)

Front 32

Complement system:

Back 32

-opsinzation

-w/infection system activated, lead sequence of events on surface of pathogen and destroy/eliminate infection.

Front 33

4 major functions of inflammation in complement system:

Back 33

C3a and C5a - mast cell release histamine

C3b - bind to cells to tag phagocytosis

C3a - recruit/activate WBCs

C5b-C9 - forms MACS & lyses microbes

Front 34

Kinin System:

Back 34

-serious of enzymes leading to conversion of plasma precursors into active polypeptides

-dilation of blood vessels

-bradykinin agent produce vascular dilation, ↑ vascular permeability

Front 35

Coagulation system:

Back 35

-thrombin: fibrin clots + endothelial activation

Front 36

products of arachidonic acid breakdown:

Back 36

-mediate inflammatory reactions

-fatty acid (responsible for inflammation in muscle tissue)

Front 37

Arachidonic acid breakdown example

Back 37

working out, muscle damage, certain enzymes flock toward affected area and free ARA from membrane.

Front 38

acute phase proteins:

Back 38

-↑ conc. in plasma during inflammation

-iron-storage protein that measure iron status

-plasma protein

Front 39

IL-8: (protein mediator)

Back 39

some attract neuclophils that attact monocytes

Front 40

chemokine alpa:

Back 40

produced by monocytes, some T lymphocytes, endothelial cells, platelets

Front 41

IL1: (protein mediator)

Back 41

-induce fever

-↓ blood pressure

-release prostagladins

-collagenas

-acute phase proteins

Front 42

TNF alpha: (protein mediator)

Back 42

-fambam of ligands

-host defense against infections

-a cytokine produced in greatest amount by stimulated macrophages

Front 43

process of mast cell in tissue to be released

Back 43

1. surface coated with receptors

2. cytoplasm loaded with granules containing mediators of inflammation

3. receptor outside bind w/ligand & trigger exocytosis of granules (move outside of mast cell)

Front 44

key players in initiation of inflammation:

Back 44

mast cells

Front 45

what activates recruiting:

it recruits what?

Back 45

-mediators

-neutrophils, lymphocytes (B T cells), eosinophils

Front 46

TNF alpha cause:

lead to:

what kind of protein is it:

Back 46

-excessive inflammation

-lead to pain and tissue damage

-signaling protein

Front 47

chemokines with adhesion molecules cause what in inflammatory:

Back 47

directional migration of leukocytes in inflammatory

Front 48

Reactive Oxygen Species (ROS) produced by:

Back 48

activated phagocytes: neutrophils + macrophages

Front 49

ROS lead to:

damages:

Back 49

-tissue injury

-other molecules and cell structure they're part of

Front 50

3 examples of ROS molecules:

Back 50

1. hydrogen peroxide ions

2. hydroxyl radicals

3. superoxide (anion + ion)

Front 51

ROS are good too because:

Back 51

the macrophages and neutrophils must generate to kill bacteria engulfed by phagocytosis (and they're released during macro+neu activated).

Front 52

3 roles of exudate:

Back 52

1. dilution

2. bacterial killing by antibody and complement

3. localization

Front 53

Bradykinin relaxes:

Back 53

smooth muscle walls of arterioles

Front 54

Bradykinin ↑ and ↓ what:

Bradykinin is like:

Back 54

- blood flow to tissue (make red/swollen)

-blood pressure

-histamine

Front 55

precursor:

Back 55

compound that participate in chem rxn that makes another compound.

Front 56

how do hageman factor make bradykinin:

Back 56

1. HF circulate blood inactive precursor

2. tissue damage, blood escape into tissue space

3. HF contact collagens inside space = actived

4. HF start cleaving prekillikrein into killinkrein

5. kallikrein cleaves kininogen forming bradykinin

Front 57

acute inflammation responds by (3):

Back 57

1. isolating damaged area

2. mobilizing effector cells/mols to site even if later

3. promote healing

Front 58

Abcess formation:

Back 58

1. center: liquefied dead tissue mixed with remain of dead neutrophils

2. fibrin & living neutrophils present

3. healthy part, proliferating fibroblasts, young collagen fibers (repair process)

Front 59

in abcess, what's good about the outer layer:

Back 59

this zone is a barrier so no more inflammation spreads

Front 60

ulcers:

Back 60

-local defect in epithelial surface cause by shedding of dead epithelial cells