Intro to acute inflam

Question 1

Inflammation

Answer 1

A protective response intended to eliminate the initial cause of cell injury as well as necrotic cells and tissues resulting from the original insult

Question 2

Inflammation is innate or adaptive

Answer 2

Innate

Question 3

Inflammatory reaction goal

Answer 3

Bring cells and molecules of host defence from the blood stream to the site of infection or damage

Question 4

Components of inflam

Answer 4

Cells and molecules that can leave the circulation (eg Neutro, lymphocytes, monocytes, platelets, plasma pros, etc)
Tissue resident cells (eg macrophages, mast cells, fibroblasts, ECM pros)
Endo and smooth muscle cells of vessel wall

Question 5

Cause of normal tissue injury

Answer 5

Inflammatory reaction and subsequent repair processes

Question 6

Pathology becomes dominant in inflam reaction if the reaction is:

Answer 6

Very strong (severe infection)
Prolonged (persistent infection)
Innapropriate (autoimmune, allergy)

Question 7

Cause of acute inflam

Answer 7

Injury of biological,
physical
Chemical
Or immunological cause

Question 8

Result of inflamm reaction

Answer 8

Damaged tissue flooded by excess fluid (exudate) (similar to plasma) escaping through altered vessel walls which dilutes and nutralises irritant chemicals. Tissue invaded by phagocytes to remove cell debris and infectious agent and immune complexes

Question 9

5 cardinal signs

Answer 9

Heat
Red
Pain
Swelling
Loss of fx

Question 10

Swelling cause

Answer 10

Exudate accum

Inflam cell migration from vessel to EC space

Question 11

Loss of fx cause

Answer 11

Pain
Cell and tissue destruction
Effect of vascular disturbance on normal fx

Question 12

Pain cause

Answer 12

Incr pressure

Release of chemicals from damaged cells - stim nerve endings

Question 13

Redness cause

Answer 13

Same as heat plus maybe incr metabolic rate of tissue cells

Question 14

Heat cause

Answer 14

Vasodilation
Incr blood flow
Intra and extra vascular accum of blood

Question 15

Vascular response

Answer 15

Active hyperaemia with changes in vessel calibre
Vessel wall changes and endo swelling
Thrombosis, pavementing, sludging

Question 16

Inflammatory oedema or exudation of fluid response

Answer 16

Incr hydrostatic pressure so incr filtration of fluid and electrolytes
Plasma pros escape through gaps in endo wall of cap and venules

Question 17

Where and how inflam mediators found

Answer 17

Widely distributed in sequestered or inact form through body, act locally at injury site.

Question 18

Mediator fxs and communication

Answer 18

Many fxs overlap and are linked via interactions to give positive feedback/ synergist effects

Question 19

Inactivation of mediators (general)

Answer 19

Rapid inact locally to five control to inflam process

Question 20

What is histamine and where found

Answer 20

Rapid acting vasoactive amine
Granules of mast cells and basophils
(Platelet equivalent = serotonin)

Question 21

Histamine effects

Answer 21

Dilate small blood vessels
Immediate incr vascular permeability
Smooth m contraction

Question 22

2 phases of incr vascular permeability

Answer 22

Immediate (histamine and serotonin)

Delayed (PGs, leukotrienes and kinins)

Question 23

What is a kinin and how are they produced

Answer 23

Biologically active polypeptide produced by kallikrein enzyme actions on kininogen

Question 24

Example of kinin and fx

Answer 24

Bradykinin

In addition to vascular effects it produces pain via an axon reflex

Question 25

C2-kinin formation

Answer 25

By plasmin enzyme or classical complement activation

Question 26

Kallikrein enzyme formation (kinins)

Answer 26

Exist in plasma as inact prekks | Act during blood clotting

Question 27

What are PGs and LTs

Answer 27

Fatty acids from phospholipids in cell mem synthed by activated cells, not stored for release PL-Archidonic acid by PLase A2 A acid - PG or thromboxane by cyclo-oxygenase or - LT by lipoxygenasr

Question 28

PG/LT effects

Answer 28

``` Delayed vasodilation Delayed incr vascular permeability Smooth m contraction (LTs) Pain Neutrophil chemotaxis (LTs) ```

Question 29

Platelet activating factor effect and synth

Answer 29

Synthed by act mast cells from mem PLs | Cause platelet degran

Question 30

Complement act and component effect

Answer 30

Act inter-related with kinin and coag cascade (plasmin) C3 and 5a cause histamine release Important in aggregate anaphylaxis and other immune lesions

Question 31

Types of Mediators released by neutrophils and their roles

Answer 31

``` Azurophilic granules (cont proteolytic and degradative enz key to tissue liquefaction and inflam amplification) Specific granules (cont pros with antibact property that cause mast cell degran ```

Question 32

Types of mediators released by platelets

Answer 32

``` Lysosomal granules (cont proteolytic enz and cationic pros) Dense bodies (cont serotonin) ```

Question 33

Peptides synth and effect

Answer 33

Exudate pro digested by proteolytic enzyme | Can cause incr vascular permeability

Question 34

Microbial product examples

Answer 34

``` Kinase Hyaluronidase Proteases Leucocidins Haemolysin Vasoactive toxins Can have influence on inflam resp dev ```

Question 35

What are and where are they found Cytokines

Answer 35

Protein mediators produced by local cells induced during and insult

Question 36

Cytokine effect

Answer 36

Para and autocrine to prod more cytokines Affect all inflam stages Induce incr vasodilation and permeability and induce proteolytic enz production

Question 37

What are chemokines and their fx

Answer 37

Proteins | Act as leukocyte attractants