Inflammation

Front 1

2 main components of inflammation

Back 1

vascular reaction + cellular reaction

Front 2

2 distinct phases of inflammation

Back 2

Acute --> minutes to days --> leukocyte emigration (neutrophils) + edema
Chronic --> months to decades --> lymphocytes + macrophages

Front 3

3 main components of acute inflammation

Back 3

1. Increased blood flow
2. Increased vascular permeability - allow protein extravasation, leukocyte movement to interstitium
3. Emigration of leukocytes - accumulation at site of injury, activation to eliminate agent

Front 4

Exudate

Back 4

inflammatory extravascular fluid that has high protein concentration, usually due to increased permeability

Front 5

Transudate

Back 5

a fluid with low protein concentration (most albumin), permeability not increased

Front 6

Edema

Back 6

excess interstitial fluid, can be either exudate or transudate

Front 7

Pus

Back 7

Purulent exudate, leukocytes (neutrophils), debris of dead cells and microbes

Front 8

Stimuli for acute inflammation

Back 8

-Infections (bacteria, viral, parasitic) + microbial toxins
-Trauma
-Physical and chemical (burns, frostbite, radiation)
-tissue necrosis
-foreign body
-immune reactions - hypersensitivity

Front 9

Vascular changes of inflammation

Back 9

Responsible for delivering cellular components (neutrophils, Ab's ) to the site of infection
Blood vessels change to allow movement of plasma proteins from circulation to site of injury

Front 10

Vasodilation

Back 10

one of earliest changes of acute inflammation
occasionally follows a transient vasoconstriction of arterioles - lasts only seconds
dilates arterioles first
As a result blood flow increases

Front 11

Increased permeability

Back 11

quickly follows vasodilation --> increases protein movement into interstitium

Front 12

Stasis

Back 12

With fluid movement as result of permeability changes, RBC concentrate in vasculature causing stasis

Front 13

Which leukocytes are present in acute inflammation

Back 13

Neutrophils

Front 14

What is a landmark of acute inflammation

Back 14

Increased vascular permebaility - exudate extravasation, decreases plasma oncotic pressure, increases tissue oncotic pressure --> edema formation

Front 15

What is the mechanism for endothelial cells to become "leaky" - increasing permeability

Back 15

ENDOTHELIAL GAPS IN VENULES - mediated via histamine, bradykinin, leukotrienes
-occurs rapidly, reversible and short lived
-capillaries and arterioles are not affected

Front 16

How does histamine affects permeability

Back 16

Causes contraction of venular endothelial cells - causes separation of intercellular junctions - increased permeability

Front 17

Direct endothelial cell injury

Back 17

Usually associated with platelet cell attachment
-necrotizing injuries
-such as severe burns
-"immediate sustained response"
-all levels of microcrculation are affected - arterioles, venules and capillaries

Front 18

Delayed prolonged leakage

Back 18

Begins after delay (2-12 hrs)
-venules and capillaries
-late appearing sunburn

Front 19

4 steps of journey of leukocytes from vessel lumen to interstitium

Back 19

Margination
Rolling
Adhesion
Transmigration (diapedesis)

Front 20

Describe normal blood flow through venules

Back 20

Axial streaming- RBC at center, plasma and leukocytes toward vessel wall

Front 21

Margination of leukocytes

Back 21

inflammation induces stasis - causing more leukocytes to gather at blood vessel wall

Front 22

Rolling of leukocytes

Back 22

Lwukocytes tumble slowly along endothelium and adhere transiently

Front 23

Adhesion of leukocytes

Back 23

Leukocytes come to rest and adhere to the wall

Front 24

Transmigration = diapedesis

Back 24

Leukocytes are regulated by adhesion molecules and chemical mediators

Front 25

4 types of adhesion receptors

Back 25

1. Selectins
2. Ig super family - ICAM + PCAM
3. Integrins - expressed on many cell types, bind to ligands
4. Mucin line glycoproteins - heparan sulfate

Front 26

Leukocyte effects

Back 26

-Increase arachidonic acid metabolites
-Increase lysosomal enzymes and activation of O2 burst
-Increase cytokines
-Leukocyte adhesion modulation

Front 27

Leukocyte receptors

Back 27

Toll like receptors - activated by microbes
Seven transmembrane
Cytokine receptors - on phagocytes

Front 28

3 steps of phagocytosis

Back 28

Recognition and attachment
Engulfment
Killing and degradation

Front 29

What converts H2O2 to HOCl

Back 29

Myeloperoxidase

Front 30

Most frequent cause of leukocyte dysfunction

Back 30

Bone marrow suppression

Front 31

Histamine comes from

Back 31

mast cells

Front 32

Histamine causes

Back 32

vasodilation
increase vascular permeability
immediate transient phase of inflammation

Front 33

Serotonin comes from

Back 33

Platelets

Front 34

Complement mostly located in

Back 34

Plasma

Front 35

Name anaphylotoxins

Back 35

C3a and C5a --> histamine

Front 36

C5a

Back 36

Chemotaxis

Front 37

C3b

Back 37

opsonin

Front 38

Activated Hageman factor initiates

Back 38

Clotting
Kinin
Fibrinolytic
COmplement