Chronic Inflammation Flashcards

1
Q
prolonged duration (weeks to months to years) in which active inflammation, tissue injury, and healing proceed simultaneously.
?
A

Chronic inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Chronic inflammation Characterized by ?

A
  1. Infiltration with macrophages, lymphocytes, and
    plasma cells
    2.Tissue destruction, induced by the products of the
    inflammatory cells.
  2. Repair, involving new vessel proliferation (angiogenesis)
    and fibrosis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Causes of chronic inflammation?

A
  1. Primary chronic inflammation 2. Progression from acute inflammation: • The persistence of the injurious agent or • Interference with the normal process of
    healing.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Causes of Primary Chronic inflammation ( i.e no initial phase of acute inflammation)?

A
  1. Persistent infections by
    microbes that are difficult to
    eradicate.
  2. 2- Immune-mediated
  3. 3- Prolonged exposure to
    potentially toxic agents.
    Eg:
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Chronic Inflammatory Cells

A

Macrophages, 2.Lymphocytes, 3.Eosinophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Two major pathways of macrophage activation ?

A
  1. Classical pathway 2. Alternative pathway
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Classical macrophage activation induced by

A

Induced by: 1. microbial products such as endotoxin, 2. T cell–derived signals, the cytokine IFN-γ, and 3. by foreign substances including crystals and particulate matter.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Classically activated macrophages produce : ?

A
  1. lysosomal enzymes, 2. NO, and 3. ROS,
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Classical macrophage activation

Work on ?

A

Ros and no and lysosome = Phagocytosis and killing of many bacteria / inflammation = iil 1 12 23 Chemokines

All of which enhance their ability to kill ingested organisms, and
secrete cytokines that stimulate inflammation.

• These macrophages are important in host defense against ingested
microbes and in many chronic inflammatory reactions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Alternative macrophage activation

Induced by?

A

Cytokines (IL-4 and IL-13, produced by T lymphocytes and other
cells, including mast cells and eosinophils.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Alternative macrophage activation

Role ?

A

tissue repair. They secrete growth factors that promote 1. angiogenesis, 2. activate fibroblasts and 3. stimulate collagen synthesis.

Il 10 =anti inflammatory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

induce macrophages to fuse into large,

multinucleate giant cells?

A

IFN-γ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Initiate the process of tissue repair and are involved in scar
formation and fibrosis.

Role of ?

A

Macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Display antigens to T lymphocytes and respond to signals from T
cells.
Role of ?

A

Macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

2.Lymphocytes properties?

A

Two types: T and B lymphocytes which migrate into

inflammatory sites by action of chemokines. Lymphocytes interact with macrophages to kill the organism .

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

3.Eosinophils properties?

A

Found in inflammatory sites around parasitic infections or as
part of immune reactions associated with allergies.

17
Q

The commonest appearances of chronic inflammation are?

A
  1. Chronic ulcer, 2. Chronic abscess cavity, 3. Thickening of the wall of a hollow viscus by fibrous tissue 4. Granulomatous inflammation,
18
Q

granuloma microscopically characterized by ?

A

aggregation of
macrophages that are transformed into epithelium-like cell
(epithelioid appearance) surrounded by a collar of mononuclear
leukocytes, principally lymphocytes and occasionally plasma
cells.
• Older granulomas develop an enclosing rim of fibroblasts and
connective tissue .

19
Q

Granulomas can form under three settings:

?

A

1- With persistent T-cell responses to certain microbes (such as Mycobacterium tuberculosis, T. pallidum, or fungi), in which T cell–derived cytokines are responsible for chronic macrophage activation.
2- In a disease of unknown etiology called sarcoidosis
3- Granulomas may develop in some immune mediated inflammatory diseases, notably Crohn disease. 4- They develop in response to relatively inert foreign bodies (e.g., suture or splinter), forming so-called foreign body granulomas

20
Q

tubercle bacillus grossly ?

A

granular, cheesy appearance called caseous necrosis.

21
Q

tubercle bacillus microscopy?

A

Necrotic material appears as amorphous, structure less,
granular debris. • Focus of activated macrophages (epithelioid cells),
rimmed by fibroblasts, lymphocytes, histiocytes,
occasional Langhans giant cells. • Central necrosis with amorphous granular debris; acid-
fast bacilli • (ziehl Neelsen stain for acid fast bacilli)

22
Q

Types of giant cells ?

A

= Langhans’ giant cells Langhans’ giant cells have a horseshoe arrangement of peripheral nuclei at one pole of the cell and are characteristically seen in tuberculosis, although they may be seen in other granulomatous conditions
= Foreign body giant cells Foreign body giant cells’ are large cells with nuclei randomly scattered throughout their cytoplasm. They are characteristically seen in relation to particulate foreign body material.

23
Q

most important

mediators of the acute-phase reaction ?

A

cytokines TNF, IL-1, and IL-6 = plasma proteins

24
Q

The acute-phase response consists of ?

A
  1. Fever:
  2. Elevated plasma levels of acute-phase proteins:
  3. Leukocytosis
  4. Other manifestations of the acute-phase response include:
  5. Chronic inflammation
  6. In severe bacterial infections (sepsis),
25
Q

High levels of TNF cause ?

A

disseminated intravascular

coagulation (DIC), hypoglycemia, and hypotensive shock.

26
Q

wasting
syndrome called cachexia, which is mainly the result of TNF
-mediated appetite suppression and mobilization of fat stores.?

A

5.Chronic inflammation is