Chronic Inflammation

Front 1

What is a hallmark of chronic inflammation?

Back 1

tissue destruction following macrophage activation

Front 2

What cell is seen in actue inflammation?

Back 2

Neutrophils

Front 3

Does all chronic inflammation lead to granuloma formation?

Back 3

NO

Front 4

Granulation Tissue

Back 4

NOT the same as a granuloma
Healing tissue of the process, new collagen, new vessels and fibroblasts

Front 5

Granuloma

Back 5

Microscopic aggregation of macrophages that are transformed into epitheliod cells
Surrounded by leukocytes, lymphocytes and plasma cells
NOT all chronic inflammation will lead to this

Front 6

Giant Cells

Back 6

Fusion of epithelioid cells/macrophages from a Granuloma
Multinucleated

Front 7

What cell can be persistant sometimes during a chronic inflammaotry repsonse?

Back 7

Neutrophils

Front 8

What interplay is happening between Lymphocytes and Macrophages?

Back 8

Macrophages are producing IL-1, TNF-A, and IL-6, the latter of which is keeping Lymphocytes active
Lymphocytes are producing IFN-G which stimulates Macrophages
Prolonged continuation of this process leads to damage

Front 9

Monocytosis

Back 9

If the percentage of monocytes in the WBC's is higher then 10-13%

Front 10

Besides TB what other disease would present Giant Cells

Back 10

Sarcoidosis

Front 11

Resolution

Back 11

Phagocytosis of dead cells and debris principally by macrophages leaving the original tissue architecture intact

Front 12

Regeneration

Back 12

Proliferation of cells replaces lost tissue three aspects considered:
Cell Types, Tissue Architecture, and Amount of Tissue Loss

Front 13

Granulation Tissue

Back 13

Capillary formation and fibroblast migration forming a loose connective tissue framework

Front 14

Role of fibroblasts

Back 14

Produce collagen to give tissue tensile strength

Front 15

Steps in the process of Angiogenesis

Back 15

1. Proteolysis - allows sprouting
2. Migration of endothelial cells
3. Proliferation of endothelial cells
4. Maturation of endothelial cells and remodeling into tubes
5. Recruitment of cells needed for small and large vessels

Front 16

Vascular Endothelial Growth Factor (VEGF)

Back 16

Secreted by Mesenchymal cells and Stromal Cells
Receptors confined to endothelial cells
Induced by Hypoxia, TGF- Aplha and Beta, PDGF
Promotes angiogenesis, increased vascular permeability; they are leaky why you get Edema

Front 17

TGF-Beta

Back 17

TGF-B1 is most dominant
Function: Promotes monocyte chemotaxis, fibroblast migration, and collagen synthesis

Front 18

PDGF

Back 18

Has dimers A and B
Stored in platlets
Functions: Promote monocyte chemotaxis, fibroblast migration, Promote COLLAGEN SYNTHESIS AND COLLAGENASE SECRETION; b/c initial collagen is NOT used overall has to be rearanged by collagenase

Front 19

EGF

Back 19

Binds to cERB1 receptor
Distributed in tissue secretions (sweat, salvia, etc.)
Functions Promotes fibroblast migration and proliferation

Front 20

FGF

Back 20

Stimulates process in a very rapid formation
IMPORTANT in new blood vessel formation, wound repair and hematopoiesis

Front 21

Role of TNF-A and IL-1

Back 21

Promote migration and proliferation of fibroblasts in granulation tissue

Front 22

Healing by first intention

Back 22

Wounds with opposed edges
Ex: surgical incistion
24 hrs: neutrophils at margins going towards clot - epidermis starts towards clot
24-48 - epithelial spurs migrate from edges - continue to lay down basement membrane
Day 3 - Neutrophils replaced by Macs - collagen fibers appear at margins
day 5 - incisional splace filled with granulation tissue - maximal angiogenesis - collagen fibrils begin to brige incision - epidermis obtains normal thickness
2 week - continued collagen accumulation - blanching process begins
1 month - scar comprises cellular connective tissue - NO inflammatory cells - covered by intact epidermis

Front 23

Healing by Seond Intention

Back 23

Wounds with seperated edges - large wounds
Parenchymal cells cannot completely fill
Abdundant granulation tissue grows in from margins

Front 24

Differences between first and second intention healing

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In second intention
Inflammatory rxn more intense - more necrotic debris and exudates to be removed
larger amounts of granulation
Wound contraction
PRESENCE OF MYOFIBROBLASTS - may be present in first as well

Front 25

How is primary or secondary intention would healing determined?

Back 25

Determined by the nature of the wound, NOT by the healing process itself

Front 26

Bone wound healing

Back 26

Heals w/o scarring
Restore normal or near normal strength

Front 27

Intestine wound healing

Back 27

Anastomosis regains strength rapidly
Surrounding intestine affected by injury

Front 28

Nerves wound healing

Back 28

Distal severed nerve degenerates
Axon can regenerate through neural sheaths - reconnecting may be random

Front 29

Accumulation of excessive collagen

Back 29

Keloid or hypertrophic scar

Front 30

Excessive Granulation Tissue

Back 30

exuberant granulation or proud flesh - Bubbbling affect looks pink

Front 31

Exuberany proliferation of fibroblasts

Back 31

Demoids or aggressive fibromatoses - maybe hyperplasia or neoplasia

Front 32

Contracture Formation

Back 32

Wound healing near joints
Often seen in after seriuous burns

Front 33

Chronic Inflammatory Fibrosis

Back 33

Maintian persistant stimulus for fibroplasia
All involve leukocyte-macrophage interaction maintaining damage-repair scenario