Ntc 2: Inflammation 1

Front 1

In general, what is inflammation?

Back 1

-the reaction of living tissue to injury
-injured tissue releases mediators into the microcirculation (circulation from the circulation from arterioles, to capillaries and then to venules)
-Inflammation causes changes in properties

Front 2

Classical signs of inflammation?

Back 2

redness, hot, swelling pain

5th not? classical sign is loss of function

Front 3

Acute inflammation: vascular changes

Back 3

Hemodynamic: pressure and flow of blood changes due to action of arterioles
-hyperemia: +blood flow to a tissue
Permeability +: venules become more permeable
-this contributes to hyperemia

Front 4

transduate
exudate
vasoactive mediator

Back 4

- fluid flowing out of the circ that is prot free
-exudate- under acute inflammation you lose some of the plasma prot
-causes endothelial retraction and gap formation

Front 5

transient vs sustained vs delayed prolonged permeability

Back 5

t: is minor and due to mast cells that release histamine (acts on both sides of the capillary bed. it causes vasodilation of arterioles(areas becomes red) and contraction of enothelial cells in venules so you get swelling)
S: more serious, ex you burn your hand on the stove
D: ex sunburn, mediators aren't released until later

Front 6

Acute inflammation: accumulation of leukocytes

Back 6

use rolling adhesion,
-endothelial cells have receptors called selectins* that bind to compounds on the leukocytes surface and initiate rolling adhesion
- after that, the leukocyte binds to integrins (beefed up selectins)
-CD31 is a mediator of the endothelial cell that makes transmigration possible (the leuko squeezing into the the extracellular space)

-neutrophils(who are usually first to arrive) secretes collagenases that dissolve the basement membrane

Front 7

pluripotent hematopoietic stem cells

Back 7

the mother cell, located in the bone marrow

Front 8

nuetrophil

Back 8

major role is phagocytosis of pathogens and release of inflammatory mediators
- aren't around for a long time (2-3 days) before others leuko's take over
- they release neutrophil extracellular trap (NET) containing anitmicrobial agents to kill pathogens. they die in the process

Front 9

Monocyte/macrophage

Back 9

-phagocytosis of bac and degradation by lysosomal enz
- production of inflam mediators to initiate, sustain and stop inflammation
-synth mole affecting: antibacterial and antiviral defenses, blood clotting, cell growth, vasc growth, tumor growth, collagen production
- initiation of the immune response
- clean up operations
- induction of general effects (fever, acute phase reactions, cachexia)
- release of compounds to have a systemic and local effect

Front 10

Eosinophil

Back 10

mostly involved in allergin reactions. very important in dealing with parasites
relavent in hypersensitivity rxns

Front 11

lymphocyte

Back 11

are b cells and t cells
release many inflammatory mediators

Front 12

platelets

Back 12

involved in coagulation
release many mediators controlling the inflammatory reaction

Front 13

Basophils

Back 13

involved in allergic rxns

Front 14

microglial vs kupffer cells

Back 14

monocytes that have slightly different functions based on tissue
m= macrophages of the brain and spinal cord
K= macrophages of the liver

Front 15

Macrophage activation (ma)

Back 15

activated by interferons (secreted by t cells nk's and other antigen presenting cells)

Front 16

different types of cytokines that reg the activity of macrophages

Back 16

classically activated macrophage = microbiciadal activity
wound healing macrophage = tissue repair
regulatory macrophage = anti-inflammatory activity

* macrophages also release cytokines as well: interleukins, chemokines, growth factors, interferons
-they have para-auto and endocine effects

Front 17

General time frame of inflamation

Back 17

edema occurs first but neutrophils will peak in the area of inflammation within 1 day

machrophage numbers rise slowly and peak at around 2 days, replacing the neutrophils

Front 18

Inflammmasome

Back 18

Responsible for the activation of the inflammatory response!
intracellular protein that detects products from dead cells and pathogens

when it is detected it changes caspase(activates IL1- a mediator for inflammation) to its active form

Front 19

Chemotaxis

Back 19

phenomenon whereby cells direct their movement according to the chemicals in the environment

Front 20

chemokines

Back 20

proteins that infuce chmeotaxis

Front 21

phagocytosis

Back 21

recognition and attatchemnt
- opsonin- mole that act as a binding enhancer for the process of phagocytosis

engulfment:

Killing and digestion: production of reactive oxygen species and lysosomal enzymes that kill the microbes