acute inflammation 1

Question 1

what is inflammation

Answer 1

protective response intended to elimimate the cause and consequence of cell injury - dilute - destory - neutralize - initiate resolution

Question 2

Mast cells produce what

Answer 2

Histamine, source of mediators..

Question 3

Lymphocytes in the vessels induce what via smooth muscle

Answer 3

Immune response

Question 4

Monocytes in the blood vessels induce what via smooth muscle

Answer 4

Macrophages which in turn allows for the elimination of microbes, dead tissue. Source of mediators(Cytokines) Role in immune response

Question 5

Polymorphonuclear leukocytes in blood vessels induce what via basement membrane

Answer 5

Elimination of microbes, dead tissues

Question 6

Plasma proteins in vessels induce what via basement membrane ?

Answer 6

Complement system so mediators of inflammation, eliminaton of microbes. Clotting factors and kininogens: mediators of inflammation

Question 7

Endothelium is source of what?

Answer 7

Source of mediators such as nitric oxide, cytokines and others

Question 8

Cell type tree 1) multipotent progenitor produces what two progenitors? 2) answer from 1) produces what things. so the first answer produces what 4 cells. second answer produces what 4 cells, some of these then have subtypes

Answer 8

One branch first Common lymphoid progenitor > NK cell, T cell, B cell, Dendritic cell Second branch *more complicated* Common myeloid generator > (one branch) Dendritic cell, monocyte > machrphage and osteoclast, neutrophil (2nd branch of second branch) > eosiniophil (3rd branch of second branch) > basophil > mast cell (4th branch of second branch) > ethryocyte, megakaryocyte > platelets

Question 9

Differences between acute and chronic inflammation

Answer 9

Acute Rapid onset, short duration, Fluid and plasma protein exudation, Neutrophil accumulation Chronic Insidious onset lasting days to years, Lymphocytes and macrophages, scarring

Question 10

What are the 5 steps in inflammation

Answer 10

recognition recruitment removal regulation resolution

Question 11

Stimuli of acute inflammation

Answer 11

infections tissue necrosis foreign bodies immune reactions

Question 12

What are the recognition and recruitment steps

Answer 12

Host encounter an injurious agent such as microbe or dead cell Recognised by PRR on phagocytes, dendritic cells, epithelial cells > chemical mediators of inflammation Vascular change > induce changes in blood vessels Cellular events > recruitement of circulating leucocytes

Question 13

Recognition 1) what cells recogninse the presence of pathogens 2) what do they express 3) what are the two types from answer 2 4) describe them

Answer 13

1) dendiriitic and phagocytes 2) express pattern recognition receptors 2) toll like receptors and inflammasome 4) Toll-like receptors- recognize patterns that are unique to bacteria, viruses and other pathogens Inflammasome- recognizes products of dead cells and some microbial products.

Question 14

Recruitment through vascular change, what is this and why

Answer 14

Rapid response designed to deliver leukocytes and plasma protein to the site of injury Vasodilation Increased permeability

Question 15

What are the factors of arteriolar vasodilation

Answer 15

Chemical mediators (histamine and NO)  Increased blood flow  Engorgement of capillary beds  Erythema (redness) and warmth - Transudate  Increased RBC concentration  Slowed blood flow

Question 16

Normal hydrostatic pressure

Answer 16

Fluid flow  From areas of high hydrostatic pressure (HP)  Leaves the arterial end of the capillary network (32mmHg)  Reabsorbed at the venous end (12mmHg)  Towards areas of high osmotic pressure  Net flow is negligible across the vascular bed

Question 17

Transudate

Answer 17

 Increased hydrostatic pressure or decreased colloid osmotic pressure  Accumulation of interstitial fluid  Ultrafiltrate  Low protein concentration, few cells

Question 18

What is increased hydrostatic oressure and what is decreased colloid osmotic pressure

Answer 18

Increased HP is venuous outflow obstruction, congetsive heart failure Decreased OP is decreased protein synthesis, eg liver diease, increased protein loss

Question 19

Vascular permeability

Answer 19

Endothelial cells line the entire blood and lymphatic vascular system, from the heart to the smallest capillary, and control the passage of materials—and the transit of white blood cells—into and out of the bloodstream.

Question 20

What happens in immediate and transiet vasoactive mediators

Answer 20

 Immediate and transient  Histamine, bradykinin, leukotrienes  Endothelial cell contraction  Short lived (minutes)

Question 21

What happens with slow prolonged vasoactive mediators

Answer 21

Slow prolonged  Changes in cytoskeleton  IL-1 and TNF  Prolonged (hours to days)

Question 22

What happens with direct injury of endotheial cells

Answer 22

.necrosis

Question 23

what is exudate

Answer 23

Increased vascular permeability, Exudate (protein rich fluid + cells)  Change in osmotic pressure  Outflow of water and ions to extravascular space  Edema-fluid accumulation in extravascular space

Question 24

what is increased vascular permeability for recruitement vascular change for the inflammation response

Answer 24

Chemical mediators (histamine, bradykinin, leukotrienes or direct injury)  Contraction or injury of endothelial cells  Exudate  Edem

Question 25

What is the stasis of vascular change

Answer 25

Stasis  Dilated small vessels and increased vascular permeability  Extravasation of fluid (transudate and exudate)  Increased RBC concentration  Slow flow

Question 26

Vascular change lymphatics

Answer 26

Intersitital fluid is normally drained by lymphatics. But during inflammation there is increased lymph flow, drained edema, drained cell, cellular debris and microbes

Question 27

What are the 4 vascular changes

Answer 27

Transiet vasoconstriction Arteriolar vasodilation Increased vascular permeability Stasis

Question 28

What are the 5 cellular changes for leukocyte recruitment

Answer 28

Margination Rollin Adesion Transmigration Migration/chemotaxis

Question 29

What is margination

Answer 29

Leukocyte recruitment Slowed blood flow stasis, leukocytes are pushed to the margins of blood vessels tumble along the endothelial surface rolling

Question 30

What is rolling a) reduces what b) mediated by c) Sialylated ogliosaccharides,

Answer 30

Weak transient adhesion, reduces rolling veloctity, mediated by selectins (bind sugars) L selections, P selectin and E selectins on endothelial cell c) Low expression levels or absent normal endothelium  Upregulated by chemical mediators in response to infection or tissue injury

Question 31

What is adhesion a) mediated by b) expressed on what c) low affinity until d) leukocyte activation results in what e) inflammatory cytokines stimulate what

Answer 31

Mediated by integrins  Expressed on leukocyte plasma membrane  Low affinity until activated by chemokines  Leukocyte activation \> clustering of itegrins \> high affinity  Inflammatory cytokines stimulate endothelial cell expression of integrin ligands (I-CAM, V-CAM)

Question 32

What is transmigration

Answer 32

Diapedesis-movement of leukocytes between cells at the intracellular junctions  Paracellular (between cells)  Intracellular (through cells) In response to chemical gradient produced at the site of inflammation Collagenases digests basement membrane

Question 33

describe theoverall process of leukocyte recruitment

Answer 33

Question 34

How does neutrophil transmigration work?

Answer 34

They extend pseudopods and insinuate themseles between endothelial cells

Question 35

Name the leukocyte molecule and major role 1) P selectin 2) E selectin 3) GlyCam1 CD34 4) ICAM-I 5) VCAM-I 6) CD31 (PECAM)

Answer 35

1) Sialyl lewis X modifed protein, rolling (neutrophils,monocytes, lymphocytes) 2) Sialyl lewis X modifed protein, rolling and adhesion (neutrophils,monocytes, lymphocytes) 3) L selectin, rolling (neutrophils, monocytes) 4) cdi/8 Integrins (LSA-I MAC-I), Adhesion, arrest, transmigration (neutrophils, monocytes lymphocytes) 5) VLA-4 integrin, Adhesion (neutrophils, monocytes, lymphocytes) 6) CD31 Pecam, Transmigration (all leukocytes)

Question 36

overall recruitement of leukocytes 1) where are leukocytes 2) migrate towards what? 3) what is chemotaxis 4) how do leukocytes move 5) what interaction?

Answer 36

1) extravascular space 2) towards infection 3) chmical gradient produced by infection and host factor sources 4) extension of pseudopods 5) receptor chemotactic ligand interaction

Question 37

which cells occur with what type of inflammation

Answer 37

neutrophils are for rapid response and die quickly whilst macrophages and monocytes liver longer

Question 38

Serous inflammation 1) what fluid 2) what type of physical appearance

Answer 38

1) watery protein poor fluid, serum 2) skin blistering, burn, membrane effusion

Question 39

Fibrinous inflammaiton 1) increasing of what 2) what molecules and deposited where 3) characterstic of inflammation of what?

Answer 39

1) increase vasc permeability 2) fibrinogen which forms fibrin which is deposited in extracellular space 3) of meninges, pericardium, pleura

Question 40

Morphology of ulceration 1) where does it occur? 2) lower extremities with what?

Answer 40

1) necrosis and inflammation, shedding of tissue, near the syrface. Mucosa of mouth, GIT, genitourinary tract 2) lower extremtiies with poor circulation

Question 41

Classic signs of inflammation overall

Answer 41

Heat - Vasodilation; increased blood flow to injured region Redness (erythema) - vasolidation and stasis (congestion/hyperemia/engorgement) Swelling - Vasodilation and vascular permeability leading to extravasation of fluid (transudate/exudate/edema) Pain - compression of tissues, direct effect of inflammatory mediators Loss of function - direct effect of injury, pain/swelling