path: inflammation

Question 1

What is inflammation?

Answer 1

A protective response of vascularized tissues to injury

Question 2

What are the 5 events of inflammation?

Answer 2

1. An offending agent located in the interstitial tissue is recognized by host cells.
2. Leukocytes and plasma proteins are recruited from the circulation to the site of injury.
3. Leukocytes and plasma proteins work together to destroy and eliminate the offending agent.
4. Reaction is controlled and terminated.
5. Damaged tissue is repaired.

Question 3

What is exudation?

Answer 3

The escape of fluid, proteins, and blood cells from the vascular system into the interstitial tissue or body cavities.

Question 4

What is edema?

Answer 4

An excess of fluid in interstitial tissue or serous cavities; it can be either an exudate or transudate.

Question 5

What is pus?

Answer 5

A purulent exudate -> rich in leukocytes (mostly neutrophils), the debris of dead cells, and microbes.

Question 6

Exudate is protein ___?

Answer 6

rich

Question 7

Transudate is protein __?

Answer 7

poor

Question 8

Is exudate cellular or hypocellular?

Answer 8

Cellular

Question 9

Is transudate cellular or hypocellular?

Answer 9

Hypocellular

Question 10

What is the cause of exudate?

Answer 10

Increase in the normal permeability of small blood vessels in an area of injury.

Question 11

What is the cause of transudate?

Answer 11

Osmotic or hydrostatic imbalances across vessels.

Question 12

What is the sequence of events in recruitment of leukocytes to sites of infection and injury?

Answer 12

Margination, Rolling, Adhesion to endothelium, Migration across endothelium and vessel wall (transmigration), Migration in tissues toward chemotactic stimulus (Chemotaxis).

Question 13

What steps occur in the lumen of a blood vessel?

Answer 13

Margination, Rolling, Adhesion to endothelium.

Question 14

Chemotaxis is mediated by what factors?

Answer 14

C5A, Leukotriene B4, IL-8, Mannose.

Question 15

How does the leukocyte bind in the rolling stage?

Answer 15

Sialyl-Lewis X-modified glycoprotein bind to P and E-selectin.

Question 16

What is the main action of the rolling stage?

Answer 16

Cut down speed of travel.

Question 17

Integrin on neutrophil surface binds to?

Answer 17

ICAM on vascular endothelial cell surface.

Question 18

During transmigration where does movement occur from and to?

Answer 18

From vessel into interstitium.

Question 19

Which impairment in leukocyte adhesion is more severe?

Answer 19

LAD-1.

Question 20

LAD-1 (Leukocyte Adhesion Deficiency) doesn’t allow what?

Answer 20

Adhesion or rolling to occur.

Question 21

What is LAD-2 deficiency?

Answer 21

Absence of sialyl-Lewis X which is the ligand for E- and P- selectins.

Question 22

What acute phase reactant protein fixes the complement and facilitates phagocytosis?

Answer 22

C-reactive protein.

Question 23

What acute phase reactant protein binds and scavenges iron?

Answer 23

Ferritin.

Question 24

What acute phase reactant protein is a coagulation factor that promotes endothelial cell repair?

Answer 24

Fibrinogen.

Question 25

What acute phase reactant protein decreases iron absorption?

Answer 25

Hepcidin.

Question 26

What acute phase reactant protein is increased in bacterial infection?

Answer 26

Procalcitonin.

Question 27

What helps produce acute phase proteins?

Answer 27

IL-6.

Question 28

What is the function of histamine?

Answer 28

Vasodilation, increased permeability of blood vessels.

Question 29

What are fever mediators?

Answer 29

IL-1, TNF, PGE2.

Question 30

What are pain mediators?

Answer 30

Substance P and bradykinin.

Question 31

Increased acute phase proteins is caused by what?

Answer 31

IL-6 secreted from the liver.

Question 32

What are bronchospasm mediators?

Answer 32

Leukotrienes.

Question 33

What are platelet aggregation mediators?

Answer 33

Thromboxane-A2.

Question 34

How is the half-life of inflammation mediators?

Answer 34

Short half lives.

Question 35

How is the half-life of neutrophils in tissue?

Answer 35

Short (1-2 days).

Question 36

The triggering of stop signals by inflammatory mediators causes a switch in type of inflammatory mediators produced from ________________ to ______________ mediators.

Answer 36

Pro-inflammatory mediators to anti-inflammatory mediators like TGF-B and IL-10 from macrophages.

Question 37

Lipoxins are generated from?

Answer 37

Arachidonic acid.

Question 38

What is the action of lipoxins?

Answer 38

Suppresses inflammation by inhibiting the recruitment of leukocytes.

Question 39

What mediates acute inflammation?

Answer 39

Neutrophils.

Question 40

What mediates chronic inflammation?

Answer 40

Macrophages and lymphocytes.

Question 41

Chronic inflammation is a response of prolonged duration such as _____________?

Answer 41

Weeks or months.

Question 42

What are the 3 features of chronic inflammation?

Answer 42

Infiltration with mononuclear cells, Tissue destruction, Repair with new vessel proliferation.

Question 43

What are 4 causes of chronic inflammation?

Answer 43

Persistent infection, Autoimmune diseases, Prolonged exposure to toxic agents, Progression from acute inflammation.

Question 44

Granulomatous inflammation is a distinctive pattern of __________________ reaction, characterized by ___________________?

Answer 44

Chronic inflammatory, Focal accumulations of macrophages.

Question 45

Why are granulomas useful defense mechanisms?

Answer 45

They wall off the offending agent.

Question 46

What is the pathogenesis of granuloma (3 steps)?

Answer 46

1. APC's present antigens to CD4+ Th cells and secrete IL-12. 2. CD4+ Th cells differentiate into TH1 cells. 3. Th1 cells secrete IFN-gamma and cause macrophage activation.

Question 47

What are common etiologies of caseating granuloma?

Answer 47

- TB - Fungal infections

Question 48

What is the morphology of a caseating granuloma?

Answer 48

Macrophages, Epithelioid cells, Multinucleated giant cells, Lymphocytes, plasma cells, Fibrous tissue at the periphery.

Question 49

What cells are the hallmark cell of granuloma?

Answer 49

Epithelioid cells.

Question 50

What type of cells are present in TB?

Answer 50

Langhans giant cells.

Question 51

What are common etiologies of non-caseating granulomas?

Answer 51

IBS- Crohn's, Sarcoidosis.

Question 52

How do structures differ between caseating and non-caseating granulomas?

Answer 52

All structures are the same except for the central necrosis in caseating granulomas.