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Patho > L4 > Flashcards

L4 Flashcards

1
Q

Chronic inflammation ? and the three processes that occurring ?

A

is a prolonged process
(weeks-months-years) in which three processes are occurring simultaneously:
1. Active inflammation
2. Tissue destruction
3. Tissue healing (repair & fibrosis)
——It is a type of inflammation characterized by prolonged duration (weeks to years) in which there is continuous inflammation, tissue injury, and healing (by fibrosis) at the same time.

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2
Q

Causes of chronic inflammation ? 3

A

Acute inflammation may progress to
chronic inflammation.

Chronic inflammation may superimposed by
acute inflammation.

Both types may overlaps.

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3
Q

Causes of chronic inflammation
Chronic inflammation can arise either: ?

A
  • As a chronic inflammation from the start.
  • As a complication of unresolved acute
    inflammation. This happen in case of following
    conditions—>next Q
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4
Q

From the Causes of chronic inflammation is the complication of unresolved acute
inflammation,This happen in case of following
conditions: ?

A
  1. Persistent or non healing acute inflammation
  2. Persistent infection caused by pathogens that cannot be readily eliminated (T.B. bacilli)
  3. Continuous exposure to exogenous influence
    (tobacco)
  4. Impaction of foreign materials
  5. Autoimmune diseases as rheumatoid arthritis and
    Immune-mediated inflammatory diseases as
    bronchial asthma
  6. Diseases of unknown origin as inflammatory
    bowel disease
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5
Q

Cells of Chronic inflammation?

A
  1. Lymphocytes: T-lymphocytes secret cytokines and B
    lymphocytes → plasma cells.
  2. Plasma cells: Form antibodies (Ig).
  3. Eosinophils –Found in parasitic infection, allergic sites.
  4. Mast cells: play role in both acute & chronic inflamm. as in
    allergy
  5. Foreign body giant cells
  6. Macrophages:
    – Dominant cell type in chronic inflammation
    – Derived from blood monocytes & tissue histiocytic
    – Scattered all over the body such as microglia, Kuepfer cells,
    sinus histiocytic, alveolar macrophages, etc.
    – Reach site of injury within 24 – 48 hrs.
    – Become activated by T cell-derived cytokines, endotoxins, and
    other products of inflammation
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6
Q

Cells of Chronic inflammation
1. Lymphocytes: ?
2. Plasma cells : ?
3. Eosinophils : ?
4.mast cells : ?
5. Foreign body giant cells

A
  1. Lymphocytes: T-lymphocytes secret cytokines and B
    lymphocytes → plasma cells.
  2. Plasma cells: Form antibodies (Ig).
  3. Eosinophils –Found in parasitic infection, allergic sites.
  4. Mast cells: play role in both acute & chronic inflamm. as in
    allergy
  5. Foreign body giant cells
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7
Q

Cells of Chronic inflammation , Macrophages? 5

A

– Dominant cell type in chronic inflammation
– Derived from blood monocytes & tissue histiocytic
– Scattered all over the body such as microglia, Kuepfer cells,
sinus histiocytic, alveolar macrophages, etc.
– Reach site of injury within 24 – 48 hrs.
– Become activated by T cell-derived cytokines, endotoxins, and
other products of inflammation

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8
Q

Functions of Macrophages? 5

A
  1. Phagocytosis of bacteria such as TB & lepra bacilli.
    (act as sensor cell)
  2. Phagocytosis of necrotic debris. (act as sensor cell)
  3. Eliminate the harmful agents (act as effector cells)
  4. Formation of giant cells with greater phagocytic
    power.
  5. Initiate healing process.
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9
Q

Macrophages can be activated by two pathways: ? 2 and explain each ?

A

 Classical pathway: Aim to eliminate the causative agent and induce
inflammation.

 Alternative pathway: aim to repair the damaged tissue.

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10
Q

What happend to macrophag After the inflammatory process subside ?

A

macrophages will be die and eliminated by the
lymphatic system.

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11
Q

Classically activated macrophage activated by ? 2

A

IFN-y
Microbes

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12
Q

Classically activated macrophage (M1) function ? And by how ? 2f

A

1-Microbicidal actions:phagocytosis and killing of many bacteria and fungi—->by ROS,NO,lysosomal enzymes

2-inflammation:by IL-1,IL-12,IL-23,chemokines

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13
Q

…….-………interactions in chronic inflammation.

A

Macrophage-lymphocyte

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14
Q

What Activated lymphocytes and macrophages do?and what they release ? 3

A

stimulate each other Both cell types release inflammatory mediators that affect other cells.
IFN-γ, interferon-γ; IL-1, interleukin 1; TNF, tumor necrosis factor.

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15
Q

Two Basic Types of Chronic Inflammation:

A
  1. Chronic Nonspecific Inflammation
  2. Chronic specific Inflammation (Granulomatous Inflammation)
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16
Q
  1. Chronic Nonspecific Inflammation ? 3
  2. A preponderance of…. + …..+……
    2-?
  3. Mediated by…? + what happend 2
A
  1. A preponderance of mononuclear cells (macrophages, lymphocytes, plasma cells) often with fibrosis and
    vascular proliferation.
  2. Fibrosis (scarring) & distortion of tissue architecture.
  3. Mediated by the interactions of
    monocytes/macrophages with lymphocytes
  4. Cytokines from macrophages activate lymphocytes which
    produce cytokines activating macrophages (+ feedback loop)
  5. B-cell activation occurs via macrophage presented antigens
    producing antigen specific plasma cell proliferation
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17
Q

Chronic specific Inflammation or …..

Definition?

A

(Granulomatous Inflammation)

A distinctive form of chronic inflammation characterized by focal accumulation of large number of activated macrophages together with lymphocytes, giant cells and fibroblasts forming tiny granules which fuse to form tumor-like masses.

18
Q

Recognition of a granuloma is?

A

of diagnostic
importance because of the limited number of
conditions that can cause it.

19
Q

Mechanism of granuloma formation 2

A

The events that give rise to formation of granulomas in type IV hypersensitivity reactions.
• Note, the role played by T-cell-derived cytokines.

20
Q

A microscopic aggregate of… cells, typically surrounded by a collar of……, is called a granuloma

A

epithelioid-lymphocytes

21
Q

macrophage activation • Activation signals include ?3

A

bacterial endotoxin,

cytokines secreted by sensitized T lymphocytes (in particular the cytokine IFN-γ),

ECM proteins such as fibronectin.

22
Q

Macrophages secrete biologically active products that can
result in the tissue injury and fibrosis that are characteristic of chronic inflammation.
• These products include: ?

A
  1. Acid and neutral proteases. mediators of tissue damage in acute
    & chronic inflammation.
  2. plasminogen activator, greatly amplify the generation of proinflammatory substances. ROS and NO, AA metabolites
    (eicosanoids)
  3. Cytokines such as IL-1 and TNF
  4. a variety of growth factors that influence the proliferation of
    smooth muscle cells and fibroblasts and the production of ECM
23
Q

Etiological classification:
1- Infective granulomas: ? 3

A

A. Bacterial: TB, leprosy and syphilis
B. Parasitic: Schistosomiasis
C. Fungal: Histoplasmosis and Blastomycosis

24
Q

Etiological classification: 2- Non-infective granulomas: ? 2

A

A. Inorganic metals and dusts: Silicosis, berylliosis B. Foreign body: Suture, cat gut, talc power and pieces of wood or glass.

25
Q

Etiological classification: 3- Granuloma of unknown origin: ? 1

A

Sarcoidosis

26
Q

Etiological classification: 4-Immune reaction against intestinal bacterial, self-antigens
1

A

self-antigens
e.g. Crohn disease (inflammatory bowel disease)

27
Q

Morphological classification:
Of granulomas ? And give eg. of each

A

• Caseating granulomas: TB, syphilitic gumma
• Non-caseating granulomas: Sarcoidosis

28
Q

What is the structure of Granulomatous Inflammatiomation , Caseating Granuloma
And Non-caseating Granuloma ?

A

All have
Fibroblasts, Lymphocytes, Macrophages,Epithelioid Cells, and Giant Cells

But Caseous Necrosis only in Caseating Granuloma

29
Q

Pathogenesis of granuloma ? 7 steeps

A

Persistent or non-degradable antigens
↓
Activation of CD4(helper)
↓
Release of cytokins (IL-2, TNF, γ-IFN)
↓
Aggregation and activation of macrophages
↓
Macrophages become Enlarged, flattened with abundant esinophilic cytoplasm
↓
Epithelioid cells
↓
Giant cells

30
Q

Note that the activated macrophage releases products that are similar to ?

A

those released by PMNs

31
Q

TB granuloma
Formation steeps ? 8

A

• Bacterial entry
• T Lymphocytes.
• Macrophages.
• Epitheloid cells.
• Proliferation.
• Central Necrosis.
• Giant cell
formation.
• Fibrosis.

32
Q

Morphology of Granuloma ? 4

A
  1. Active macrophages - epithelioid
    cells.
  2. Central Caseous necrosis.
  3. Outer layer of lymphocytes,
    plasma cells & fibroblasts.
  4. Langhans giant cells – joined
    epithelioid cells.
33
Q

Giant cells are ?

A

a “committee” of epithelioid macrophages.

34
Q

Granulomatous inflammation
Non caseating granuloma made of ?

A

each made up of an aggregate of epithelioid cells and surrounded by lymphocytes. The granuloma in the center shows several multinucleate giant cells.

35
Q

A typical caseating granuloma
Made of ?

A

resulting from infection with Mycobacterium
tuberculosis showing central caseous necrosis, activated epithelioid macrophages, many giant cells, and a peripheral accumulation of lymphocytes.

36
Q

Sarcoidosis typically presents with ??

A

non-caseating granulomas.

37
Q

Tuberculous granulomas in Early condition ?

A

(Non-caseating granuloma)

38
Q

Tuberculous granulomas Late condition?

A

(caseating granuloma) caseation necrosis

39
Q

Don’t forget that tuberculosis is not the only cause of granulomas.

A

granulomas due to schistosomiasis in the liver (Bilharziasis). Bilharzial granuloma

Fungal granuloma

Vocal cord granuloma

Etiology:
colonic Crohn disease
tuberculous colitis
colonic sarcoidosis

40
Q

Fate Of Granulomas ?

A

Granulomas may either involute (resolve rarely occur) or undergo fibrosis.

• Fibrosis usually begins at the periphery of the
granuloma and progresses towards the center, ultimately resulting in formation of a scar referred to as “tombstone lesions”.

• Foci of dystrophic calcification, either small
and discrete or plaque-like may occur in such scars.

41
Q

Summary (GRANULOMA)

A

The macrophages adhere closely and assume
epithelial shape forming epitheliod cells. Some of which fuses to form giant cell,
• They assume a nodular morphology and are called granuloma.
• Healing of granulomas is accompanied by fibrosis
that may be extensive & cause organ dysfunction in some diseases, such as tuberculosis.
• Tuberculosis is the prototype of a granulomatous
disease caused by infection and should always be excluded as the cause when granulomas are identified.

Patho (11 decks)

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