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chronic inflammation Flashcards

1
Q

what is the reason of chronic inflammation?

A

Chronic local inflammation is due to nondegradable pathogens, prolonged exposure to toxic pathogens, or autoimmune reactions.
It results from a balance between progressive tissue damage caused by a persistent damaging stimulus and attempted eradication of the damaging agent followed by tissue repair

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2
Q

chronic inflammation is preceded by acute inflammation. True/False.

A

True

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3
Q

chronic inflammation begins insidiously. True/False

A

True

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4
Q

how acute inflammation progress to chronic inflammation?

A

1) progression of acute inflammation
- -organization of an abscess
- - the presence of indigestible material (surgical sutures)
2) recurrent episodes of acute inflammation

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5
Q

give example when recurrent episodes of acute inflammation progress to chronic?

A

recurrent bouts of acute cholecystitis progressing to chronic cholecystitis

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6
Q

give examples of acute inflammation progressing to chronic by the organization of to an abscess

A

acute osteomyelitis progressing to chronic

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7
Q

list persistent infections that lead to chronic inflammation

A

1) Mycobacterium Tuberculosis
2) TreponemaPallidum
3) Fungi

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8
Q

prolonged exposure to what toxic agents lead to chronic inflammation?

A

silica

asbestos

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9
Q

what immunologic diseases result in chronic inflammation?

A

autoimmune diseases:Rheumatoid arhtritis, systemic lupus erythematosis

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10
Q

what are the cells involved in chronic inflammation?

A

mononuclear cells (monocytes, macrophages, lymphocytes, plasma cells), fibroblasts

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11
Q

what are the morphological features of chronic inflammation?

A
  • -Infiltration with mononuclear inflammatory cells (macrophages, lymphocytes and plasma cells)
  • -Tissue destruction (due to persistent injury/inflammation)
  • -Repair-granulation tissue (angiogenesis and fibrosis)
  • -Leads to necrosis and fibrosis (simultaneous destruction and formation of new tissue)
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12
Q

how healing occurs in chronic inflammation?

A

attempts at healing by connective tissue replacement, accomplished by vascular proliferation

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13
Q

what is the dominant cell involved in chronic inflammation?

A

macrophage

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14
Q

macrophages are derived from…

A

blood monocytes

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15
Q

list the macrophages located in different tissues (skin, liver, brain)

A

1) Kupffer cells (liver)
2) Sinus histiocytes (spleen and lymph nodes)
3) Alveolar macrophages (lung)
4) Microglia (CNS)
5) Osteoclasts (bone)
6) Langerhans cells (skin)

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16
Q

what are the 2 ways of macrophage activation?

A

1) Classical (proinflammatory): mediated by Th1 cells secreting IFN-γ
2) Alternative (anti-inflammatory): mediated by Th2 cells secreting IL-4 and IL-13, produce mediators to drive wound repair by causing fibroblast proliferation, connective tissue production, and angiogenesis.

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17
Q

the classical pathway of macrophage activation is driven by?

A

Th1 cells secreting IFN-γ

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18
Q

Alternative (anti-inflammatory) of macrophage activation is driven by?

A

Th2 cells secreting IL-4 and IL-13

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19
Q

what are the outcomes of chronic inflammation?

A
  • Scarring
  • Amyloidosis
  • Neoplasia (e.g., chronic HCV infection → chronic hepatitis → hepatocellular carcinoma)
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20
Q

describe the role of T lymphocytes in chronic inflammation?

A

1) T cells produced in the bone marrow
2) Maturation in the thymus: TCR rearrangement
3) CD4 helper cells- Major Histocompatibility Complex (MHC) class II
4) CD8 cytotoxic cells- MHC class I
5) Activation of T cells requires binding of Ag/MHC
6) T lymphocytes release lymphokines

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21
Q

where T cells are produced

1) bone marrow
2) thymus

A

T cells are produced in the bone marrow but undergo

maturation in the thymus

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22
Q

what is TCR?

A

-T-cell receptors (TCRs)
-Binding of a T-cell receptor to its specific antigen triggers activation of the T cell.
-This antigen fragment has to bind to the major histocompatibility complex molecule on the surface of -another cell in order to be recognized by the TCR.
The adaptive immune response is initiated in secondary lymphoid organs, where antigens are presented on the surface of antigen-presenting cells (i.e., macrophages, dendritic cells, B cells).

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23
Q

what is V(D)J rearrangement? (TCR rearrangement)

A

A process in which different parts of the variable (V), diversity (D), and joining (J) gene segments are brought together by site-specific recombination to produce immunoglobulin heavy chains or T-cell receptors. V(D)J recombination is an antigen-independent process that is involved in the generation of antibody and T-cell receptor diversity.

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24
Q

CD4 T helper cells are activated by MHC
1) I
2 )II

A

MHC II

MHC I activate CD8 T cells

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25
Q

describe MHC 2

A
  • -Major histocompatibility complex class II (MHC class II)
    1) Located on the surface of antigen‑presenting cells (APCs; dendritic cells, monocytes/macrophages, B lymphocytes): encoded in HLA‑DR, HLA‑DP, and HLA‑DQ
    2) Comprised of two polypeptide chains of equal length (alpha and beta) that each contains two domains (α1, α2, and β1, β2)
    3) Antigen-presenting cells can ingest exogenous material (extracellular pathogens) into fragments via phagocytosis and present them on the cell surface via MHC class II receptors.
    4) MHC II-antigen complexes are assembled in acidified endosomes after the release of the invariant chain.
    5) Antigen presentation leads to the activation of CD4+ T lymphocytes, which then activate B lymphocytes and, thus, provides a connection between innate and adaptive immunity.
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26
Q

describe MHC

A

1) Located on the surface of all nucleated body cells and platelets
2) Encoded in HLA‑A, HLA‑B, and HLA‑C
3) Comprised of two polypeptide chains of different length: The long-chain contains the alpha domains (α1, α2, α3), the short-chain is the peptide β2-microglobulin and carries the β2 domain.
4) Continuously presents endogenous fragments of proteins located in the cell, which allows for rapid detection and destruction of cells in infections with intracellular pathogens (e.g., viruses) and cells that produce atypical proteins (neoplastic or malignant cells) → cytotoxic T‑cell reaction
5) The exception is the cross-presentation of extracellular antigens by dendritic cells → primes CD8+ T cells, which can only interact with MHC I
6) Antigens are peptides, lipids, or polysaccharides which are transported to the RER via transporter associated with antigen processing (TAP).
7) MHC I-antigen complexes are assembled in the RER.
8) The polymorphic zone presents antigens derived from within the cell. The nonpolymorphic zone binds to CD8 T lymphocytes.
9) Several viruses prevent the expression of MHC class I on the cell surface. The absence of MHC class I receptors on infected or malignant cells is recognized by natural killer cells (NK cells).

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27
Q

what are lymphokines?

A

A group of proteins that mediate the immune response (e.g., chemotaxis of inflammatory mediators, antibody production, sensitization to antigens). Also implicated in the development of type IV hypersensitivity reactions. Produced by T cells.

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28
Q

describe the role of B cells in chronic inflammation

A
  • -B cells are produced in the bone marrow
  • -Activation à plasma cells ( secretes monoclonal immunoglobulins, predominately IgM, but also IgA, IgE, IgG, that target a specific antigen)
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29
Q

what are eosinophils?

A

1) Common in many allergic inflammatory reactions (mediated by IgE and parasitic infections)
2) Effective killers of parasites
3) Recruitment depends on eotaxin.
4) Phagocytic (limited)
5) Have granules containing major Basic Protein (MBP is toxic to parasites and contributes to tissue damage as it lyses mammalian epithelium)
6) Mediate tissue damage

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30
Q

which substance attracts eosinophils to the site of inflammation?

A

histamine

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31
Q

eosinophils are defensive against?

A

The immune response against parasites

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32
Q

which cytokine is responsible for the activation and proliferation of eosinophils?

A

IL-5

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33
Q

describe proinflammatory and anti-inflammatory cytokines

A

1) Proinflammatory cytokines (Th1 cytokines): stimulate the immune system
- Interleukins 1, 6, 8, 12, 18, IFN-γ, and tumor necrosis factor
- Induce fever, inflammation, and tissue destruction in response to infection, injury, or ischemia
- Uncontrolled action is deleterious and can lead to multiorgan dysfunction
2) Anti-inflammatory cytokines (Th2 cytokines): suppress the immune system
- Interleukins 4,10, 11,13, TGFβ, and receptor antagonists of IL-1 and TNFα
- Suppress proinflammatory cytokine secretion and inhibit binding of proinflammatory cytokines to their receptors
- An imbalance between the pro-inflammatory and anti-inflammatory cytokine response is responsible for several immune-mediated diseases (e.g., rheumatoid arthritis, inflammatory bowel disease, multiple sclerosis).

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34
Q

what is major basic protein?

A
  • Major basic protein: produced by eosinophils in response to antibody-dependent processes (IgE, antibody-dependent cell-mediated cytotoxicity) and important in the defense against helminthic infections.
  • IgE coat pathogens → recognized by Fc receptor-bearing granulocytes (eosinophils) → release of major basic protein → destruction of the pathogen
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35
Q

what is granulomatous inflammation?

A

1)A specific form of chronic inflammation
2)Characterized by focal accumulations of activated macrophages (granulomas)
If the immune system is unable to completely eliminate a foreign substance (e.g., persistent pathogen, foreign body), the resulting granulomatous inflammation attempts to wall off the foreign substance within granulomas without completely degrading or eradicating it.

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36
Q

what is the pathophysiology of granulomatous inflammation?

A

Antigen-presenting cells present antigens to CD4+ Th cells and secrete IL-12 → stimulate differentiation into Th1 cells → Th1 cells activate macrophages by secreting IFN-γ → macrophages release cytokines (e.g., TNF), which stimulates the formation of epithelioid macrophages and giant cells
Epithelioid cells secrete TNF-α, which serves to maintain the granuloma.
Macrophages within the granuloma ↑ calcitriol (1,25-[OH]2 vitamin D3) activation → hypercalcemia

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37
Q

what are epithelioid macrophages?

A

-A type of macrophage that resembles epithelial cells —-Can fuse together to form Langhans giant cells (multinucleated giant cells), which are components of granulomas (e.g., in tuberculosis).

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38
Q

describe the histology of granuloma

A
    • a nodular collection of central macrophages, epithelioid cells, and giant cells, surrounded by fibroblasts and lymphocytes
  • -Giant cells contain:
    1) Asteroid bodies: a star-shaped, eosinophilic inclusion body consisting of various lipids (e.g., from sarcoidosis, foreign body reactions)
    2) Schaumann bodies: a type of cellular inclusion body consisting of intracytoplasmic calcium and protein with laminar stratification (e.g., sarcoidosis, tuberculosis, Crohn disease, berylliosis)
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39
Q

describe 2 types of granuloma

A

1) Caseating granulomas: granulomas with central necrosis
- -Occurrence: infections (e.g., tuberculosis, fungal infections)
2) Non-caseating granulomatous inflammation: granulomas without central necrosis
- -Occurrence: immune-mediated diseases (e.g., sarcoidosis, Crohn disease), vasculitis, foreign body exposure

40
Q

what are the infectious causes of granulomas?

A
  • Tuberculosis
  • Fungal infections (e.g., histoplasmosis)
  • Bartonella henselae (cat scratch disease)
  • Listeria monocytogenes (granulomatosis infantiseptica)
  • Treponema pallidum (tertiary syphilis)
  • Schistosoma parasites (schistosomiasis)
41
Q

what are the immune-mediated causes of granulomas?

A
  • Sarcoidosis
  • Crohn disease
  • Subacute thyroiditis (de Quervain)
  • Primary biliary cholangitis
42
Q

vasculitis can result in granuloma formation.True/False

A

True.

  • Granulomatosis with polyangiitis
  • Eosinophilic granulomatosis with polyangiitis (Churg-Strauss)
  • Giant cell arteritis (temporal arteritis)
  • Takayasu arteritis
43
Q

foreign bodies can result in granuloma formation. True/False

A

True.

  • Berylliosis
  • Talcosis
  • Hypersensitivity pneumonitis
  • Breast implants
  • Penetrating trauma with glass, wood, etc.
44
Q

describe foreign body granuloma

A

–It occurs in response to poorly digestible foreign material
1)Exogenous
• Splinter
• Suture
• Graft material
2)Endogenous
• Keratin
• Hair shafts in pilonidal sinus
–Incited by particles that can’t be readily phagocytosed by a single macrophage but do not elicit a specific immune response (suture or talc).

45
Q

granuloma formation is what type of hypersensitivity reaction?

A

-Interactions between CD4 T helper cells and macrophages
-Macrophages present Ags via MHC II to CD4 helper cells causing their activation
-T cells produce cytokines (IL-2 and IFN-γ)
• TB
• Fungal infection
• Sarcoidosis

46
Q

which cytokines promote granuloma formation?

A

IL-2 and IFN-γ

47
Q

describe the histology of foreign body granuloma

A
  • Macrophages cluster around the foreign material

- Multinucleated giant cells with haphazardly arranged nuclei throughout the cytoplasm

48
Q

caseous necrosis seen in TB is due to what type of hypersensitivity reaction?

A

type 4 (delayed) hypersensitivity reaction

49
Q

what organs are the main site or MTB infection?

A

 Lungs and lymph nodes are the main sites of infection

50
Q

what are the histological features of caseating granuloma?

A
  • Central necrosis
  • Epithelioid macrophages and Langhans ’giant cells
  • T-helper cells (within the granuloma)
  • Occasional plasma cells
  • A peripheral rim of suppressor T cells and fibroblasts
51
Q

what stain is used in evaluation of caseous granuloma?

A

Ziehl-Nielsen for MTB

52
Q

what is sarcoidosis?

A

An idiopathic, chronic inflammatory disease characterized by the formation of noncaseating granulomas, typically in the lung and, less commonly, in the liver, eyes, and skin. Predominantly occurs in young, African-American women. A chest x-ray often reveals bilateral hilar adenopathy. A biopsy is the gold standard for diagnosis. First-line treatment is corticosteroids.

53
Q

what are Schaumann bodies

A

Round calcium and protein inclusions in the cytoplasm with laminar stratification, seen in granulomas of sarcoidosis

54
Q

what are asteroid bodies?

A

a star-shaped, eosinophilic inclusion body consisting of various lipids (e.g., from sarcoidosis, foreign body reactions)

55
Q

what are the morphologic patterns seen in acute and chronic inflammation

A
  • Serous inflammation
  • Fibrinous inflammation
  • Suppurative inflammation
  • Ulcers
  • Sinus
  • Fistula
56
Q

what is serous inflammation?

A

inflammation with a thin and watery fluid that lacks fibrinogen and fibrin. It can be seen in viral serositis as well as in skin inflammation (e.g., blisters). It is derived from the blood serum or secretion of the mesothelial lining (this is called an effusion)

57
Q

give examples of serous inflammation

A 
1)Effusion
•Peritoneal
•Pleural
•Pericardial 
2)Skin blisters (the skin blister resulting from a burn or viral infection represents a large accumulation of serous fluid, either immediately beneath or within the epidermis.)
3)Viral infection
4)Burn
58
Q

the viral infection is characterized by suppurative or serous inflammation?

A

serous

59
Q

burns are characterized by serous or fibrinous inflammation?

A

serous

60
Q

what is fibrinous inflammation?

A

Due to an increase in vascular permeability, large molecules such as fibrinogen pass the barrier and fibrin are formed and deposited at in extracellular pace.
-Accumulation of fluid and fibrin
-Body cavities
-May be removed by fibrinolysis (resolution)
-Organisation
Fibrous exudate is characteristic of inflammation in linings of body cavities (meninges, pericardium).

61
Q

fibrinous inflammation is characteristic of what?

A

Fibrous exudate is characteristic of inflammation in linings of body cavities (meninges, pericardium)

62
Q

how fibrin in fibrinous inflammation is removed?

A

by fibrinolysis
–Since the fibrinolytic system continuously cleaves and degrades fibrin, hemostasis, and fibrinolysis are processes that occur simultaneously in the circulatory system.
–Physiological fibrinolysis
Tissue injury → release of factor XII, urokinase and tissue plasminogen activator (tPA)
→ Breakdown of plasminogen, leading to the formation of active plasmin → breakdown of fibrin by activated plasmin
→ Release of degradation products, including D-dimers
Regulation of fibrinolysis: tPA activity is reduced if tPA binds to plasminogen activator inhibitor (PAI).

63
Q

what is suppurative inflammation?

A

-A descriptor for conditions that cause inflammation and the production of purulent exudate (e.g., cutaneous infections).

64
Q

suppurative inflammation is characterized by??

A
  • Characterised by large amounts of pus
  • Can be seen in association with certain organisms (staphylococcus)
  • May lead to abscess formation
65
Q

how an abscess is formed?

A
  • -inflammation → pus formation and tissue necrosis
  • -The focus of necrosis is separated from healthy tissues by a fibrous capsule.
  • -have a central region that appears as amass of necrotic leukocytes and dead cells
66
Q

what is an ulcer?

A

1) An ulcer is formed when the surface covering an organ or tissue is lost due to necrosis and is replaced by inflammatory tissue (sloughing off of inflamed tissue).
2) Local defect in an epithelial surface(can only occur tissue necrosis and resulting inflammation near the surface such as mucosa of the mouth)
3) Produced by shedding of dead epithelial cells
4) Skin and mucosal surfaces e.g. peptic ulcer
5) They are distinguished from erosions by the extent of tissue loss

67
Q

an ulcer occurs only on organs covered with epithelial tissue.True/False.

A

True

68
Q

what is erosion?

A

A morphologic descriptor used to describe several types of lesions. In dermatology, refers to a loss of a portion of or all of the epidermis. In gastroenterology, refers to a superficial mucosal lesion with intact muscularis mucosae. In dentistry, refers to a loss of tooth enamel.

69
Q

what are the 2 types of ulcers?

A

1) Acute
- Loss of the full thickness of the epithelium
- May or may not be associated with scarring at the base of the ulcer
- Base consisting of fibrin and debris

2) Chronic ulcers
- Usually deep penetrating
- Always associated with scarring at the base of the ulcer

70
Q

the base of the acute ulcer is composed of

A

fibrin and tissue debris

71
Q

the base of the chronic ulcer is composed of

A

Always associated with scarring at the base of the ulcer

72
Q

what is a sinus?

A
  • Tract lined by granulation tissue leading from a chronically inflamed cavity to a surface
    1) “Sinuses associated with osteomyelitis” (inflammation of the bone)
    2) “Pilonidal sinus”(nest of hairs)
73
Q

sinuses are covered by what type of tissue?

A

granulation tissue

74
Q

what is a pilonidal cyst?

A

A pilonidal cyst (intergluteal pilonidal disease) is a skin condition caused by local inflammation of the superior midline gluteal cleft, which may progress to a local abscess or fistula. It is currently hypothesized to be an acquired condition with local penetration of hair follicles and debris in stretched intergluteal pores. Affected individuals – typically obese, sedentary men with excessive body hair and a deep gluteal cleft – may be asymptomatic or present with mild local symptoms such as local oozing or erythema; however, abscesses can also cause severe pain. Pilonidal cysts are diagnosed based on patient history and clinical examination. To treat the condition, radical resection with secondary wound healing is usually necessary. Asymptomatic patients can be treated conservatively.

75
Q

what is a fistula?

A

An abnormal connection between two epithelium-lined surfaces. Examples include gastrocolic fistula, pancreaticoduodenal fistula, and arteriovenous fistula. It can be surgically created (e.g., an arteriovenous fistula created for hemodialysis access) or occur as a complication of trauma or a disease process.

  • Gastrointestinal fistula in Crohn’s disease (acquired fistula)
  • Tracheo-oesophageal fistula (congenital fistula)
76
Q

give examples of congenital fistula

A

tracheoesophageal fistula

77
Q

what is acute phase response (reaction)

A
  • The acute phase reaction is the initial response of the organism to systemic or local disturbances (e.g., operation, trauma, inflammation, infection, malignancy).
  • It provides rapid protection for the host by destroying pathogens and promoting the healing processes. Part of this response is the release of more than 30 acute phase reactants, which are produced in the liver and leukocytes.
78
Q

give example of acute-phase reaction

A

SIRS (systemic inflammatory response syndrome)

79
Q

what is the acute phase response 1?

A

pyrexia (fever)

80
Q

what is the pathophysiology of pyrexia?

A
  1. Temperature elevation occurs in response to Pyrogens (substances that stimulate PG synthesis in the hypothalamus).
  2. The endotoxin stimulates the leukocyte release of IL-1 and TNF-a that increases COX production of prostaglandins.
  3. In the hypothalamus, PGE2 stimulates secondary signals that reset the temperature set point.
81
Q

which prostaglandin reset temperature set point in the hypothalamus

A

PGE2 (synthesized in the hypothalamus!!!!!!!)

82
Q

which cytokines cross the blood-brain barrier and stimulate prostaglandin formation in the hypothalamus?

A

IL-1 and TNF-a

83
Q

how IL-1 and TNF-a increase prostaglandin formation in the hypothalamus?

A

by overexpressing COX enzymes

84
Q

Acute-phase response- 2 is due to

A

Acute-phase proteins

85
Q

give examples of acute-phase proteins

A
  • C-reactive protein (CRP)
  • serum amyloid A (SAA)
  • Fibrinogen à binds to RBCà ↑ESR (erythrocyte sedimentation rate)
  • Iron regulating peptide- hepcidinà reduce the availability of iron àiron-deficiency anemia associated with chronic inflammation (AOCD)
  • ferritin
  • α1-Antitrypsin → protection from protease activity
  • Serum amyloid A
  • IL-6
86
Q

what is the role of CRP?

A

-promotes opsonization of pathogens
-Increases the capacity of macrophages to phagocytose
-High sensitivity for detecting inflammation
-In bacterial infections, especially marked increase
-Increases about 6–12 hours after the
the inflammatory process begins
-Half-life of 24 hours
-Not specific to any disease or organ

87
Q

what is the role of ferritin

A
  • protein that stores and releases iron
  • Serum ferritin levels increase in the case of an infection or malignancy to reduce the amount of free iron available to pathogens or tumor cells, respectively.
  • In contrast, some organisms (e.g., Pseudomonas) cause serum ferritin levels to drop.
88
Q

describe acute phase response 3

A
  • is the same as leukocytosis
  • due to accelerated release of bone marrow cells., typically with immature neutrophils in the blood (shift to left). Shift to left means a high number of immature cells.
  • Usually 4-8 (per microliter of blood)  rises to 15-20
  • Bacterial infections = neutrophilia
  • Parasites = eosinophilia
  • Viruses = lymphocytosis (increased lymphocyte numbers)
  • Certain infections (some viruses) = induce leucopenia (decreasing number of WBCs)
89
Q

what is a leukemoid reaction?

A

A persistent leukocytosis > 50,000 cells/mm³ that is caused by reactive proliferation within the bone marrow (typically of myeloid elements) and elevated LAP in response to stress or infection.

90
Q

what is a LAP score?

A

An enzyme found in mature leukocytes. The staining of LAP on a peripheral blood smear is used to calculate the LAP score. A high LAP score is associated with an increased number of mature white blood cells (e.g., from leukemoid reaction or myeloproliferative disorders); a low LAP score is associated with an increased number of immature white blood cells (e.g., from CML).

91
Q

what cells are increased in the blood in the case of parasitic infections?

A

eosinophils

92
Q

what is an acute-phase reaction 4

A

-Increased pulse and blood pressure
-Decreased sweating and rigors (due to redirection of blood flow from cutaneous to deep vascular beds, to minimize heat loss through the skin)
-Tendency to sleep
-Anorexia and malaise (due to action of cytokines on brain cells)
-Severe sepsis – DIC, hypotension, and shock
In severe bacterial infections (sepsis), the large number of organisms and LPS in blood stimulate the production of large amounts of cytokines (mostly TNF and IL-1) –these cause clinical manifestations such as disseminated intravascular coagulation, cardiac failure, and shock.

93
Q

what is the pathophysiology of decreased sweating and rigors?

A

due to redirection of blood flow from cutaneous to deep vascular beds, to minimize heat loss through the skin

94
Q

which cytokine is responsible for anorexia and malaise?

A

TNF-alfa

95
Q

which substance of bacteria stimulates the production of large amounts of TNF-alfa and IL-1 causing shock?

A

lipopolysaccharide of G- bacteria (endotoxin)

although in clinical practice the most common cause of sepsis is G+ bacteria

General Pathology (9 decks)

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