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Pathology > Chronic inflammation > Flashcards

Chronic inflammation Flashcards

1
Q

Chronic Inflammation

A
  • prolonged duration
  • accompanied by tissue destruction & repair by fibrosis (healing & repair) proceeding simultaneously
  • occur after acute inflamm
  • insidious w/ no acute inflamm phase

ex.

rheumatoid arthritis, atherosclerosis, tuberculosis & pulm fibrosis

neoplasia & AD

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2
Q

Causes

A
  1. peristen infection- Treponema pallidum or mycobacteria (delayed hypersensitivity)
  2. autoimmune disease- rheumatoid arthritis, MS, allergic disease
  3. prolonged exposure to toxic agents- silicosis & atherosclerosis (endogenous toxic lipids)
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3
Q

Morphology

A
  • infiltrate w/ mononuclear cells like macrophages, lymphocytes & plasma cells
  • tissue destruction, induced by the products of inflammatory cells
  • repair, involving new vessel prolif (angiogenesis) & fibrosis
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4
Q

Comparing inflamm

A
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5
Q

Inflammation

A
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6
Q

Cells

A

from BM

Chronic= macrophages, lymphocytes, plasma cells (have months to years half life)

Myeloid lineage

  • neutrophils in acute
  • eosinophils
  • mast cells/ in tissue basophils
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7
Q

Macrophage

A
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8
Q

Macrophages

A
  1. kupffer cells- liver
  2. alveolar macrophages- lung
  3. histiocytes- CT
  4. fixed & free- in spleen & LN
  5. microglial cells- nervous sys
  6. osteoclasts- bone
  7. langerhans’ cells- skin
  8. dendritic cells- lymphoid tissue
  9. epithelioid histiocytes- granulomas
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9
Q

Macrophage

A

abundant cytoplasm & vesicular, bean shaped nuclei

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10
Q

Immunity

A
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11
Q

Activate Macrophages

A
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12
Q

Plasma Cells

A

Clock face

Coarse chromatin

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13
Q

Immune Rxn Cells

A

IgE

eosinophils- IgE, parasitic infection

  • major basic prot
  • recruited by eotaxin
  • allergic rxn

mast cells

  • allergic condition, anaphylactic rxn via IgE
  • control inflamm rxns
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14
Q

Mast Cells

A
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15
Q

Eosinophils

A
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16
Q

Granulomatous inflammation

A
  • granulomas- aggregates of modified macrophages, epithelioid cells or histiocytes w/ zone of lymphocytes & fibrosis
  • multinucleated giant cells
  • caseous necrosis in TB
  • non necrotizing in sarcoidosis
  • healing granuloma’s produce fibrosis
17
Q

Cascerous necrois

A
18
Q

Epithelioid Histiocytes

A

Always around center of granuloma

look like a foot print

Activated macrophages resembling epithelial cells

19
Q

Foreign Body Granuloma

A

Form giant cells

foreign body like hair, food particle, keratin, cholesterol, suture

this is cholesterol example

20
Q

Foreign Body Giant Cell lung

A
21
Q

Suture

A
22
Q

Immune Granuloma

A
  1. macrophage engulf bac
  2. process & present bac infectious againt Ag w/ MHC II
  3. complex activates CD4+ T cells
  4. CD4 secrete IFN-g
  5. causes prolif & recruitment of modified macrophages- epithelioid histiocytic cells
23
Q

Caseating Granuloa TB

A
24
Q

Cat Scratch Disease

A

non caseating geographic stellate necrotizing granulomata

25
Q

Non caseating Non necrotizing Granuloma sarcoid

A

immune disease

usually in african americans

Cannot have TB!

26
Q

Specific Infections w/ granuloma

A
  1. TB
  2. leprosy
  3. brucellosis
  4. histoplasmosis
  5. parasites- schistosomiasis
  6. cat scratch disease
27
Q

Foreign Bodies w/ granuloma

A

Endogenous- keratin & uric acid crystals in gout

Exogenous- silica, asbestos dust, talc, suture material, silicone, prostheses

28
Q

Further issues w/ granulomas

A
  1. beryllium in body
  2. hepatic granuloma due to allopurinol, phenylbutazone, sulphanomides
  3. sarcoidosis, Crohn disease
29
Q

Acute phase Response

A

Clinical features

  1. fever
  2. increased pulse & bp
  3. decreased sweating
  4. rigors & chills
  5. somnolence
  6. anorexia & malaise
  7. septic shock
30
Q

Acute Phase Response

A

Acute phase prot

  • c reactive prot
  • fibrinogen
  • serum amyloid A prot

Leukocytosis

  • neutrophilia
  • eosinophilia
  • lymphocytosis

Leukopenia

31
Q

Fever

A
  • pyrogens increase hypothal PG production
  • Cause by LPS
  • lead to increase in IL-1 & TNF
  • upreg cyclooxygenases to increase PG
  • cAMP NT produce reset in temp
  • help ward off infection
32
Q

Increase pulse & BP, decrease sweating

A

ANS adrenergic effect

33
Q

Rigors, chills, anorexia, malaise, somnolence

A

actions of cytokines on brain

34
Q

Sepsis fromm organisms & LPS

A

increase iN TNF, IL-1

DIC, hypoglycemia, hypotensive shock

35
Q

Acute Phase Proteins

A
  1. mannose binding prot- opsonization & complement activation
  2. c reactive prot- opsonization
  3. a1 antitrypsin- serine protease inhibitor
  4. haptoglobin- binds Hg
  5. ceruloplasmin- antiox, binds Cu
  6. fibriongen- coagulation, erythrocyte sedimentation rate ESR
  7. Serum amyloid A prot- apolipoprot replacement in HDL directs lipids to histiocytes
  8. a2 macroglobulin- antiprotease
  9. cysteine protease inhibitor- antiprotease
36
Q

CBC

A
  1. bac infection- neutrophilia
  2. parasitic infection- eosinophilia
  3. viral- lymphocytes

leukemoid rxn: 40-100,000 ul/mL w/ neutrophila shift to immature form due to TNF & IL-1 cytokines

malaria- increase monocyte, lymphocytes

37
Q

Leukopenia in infection

A
  • decreased WBC
  • typhoid fever & viral infections, rickettsia, protozoal infections
  • due to sequestered lymphocyte in LN
  • overwhelming infection– disseminated cancer, rampant TB & alcoholism
38
Q

Defective Inflamm

A
  • increased susceptibility to infections- innate immunity
  • delayed healing of wounds
  • tissue damage increase due to:
  • isolating damaged area
  • mobilize effector cells & molecs to site
  • promoting healing & repair

Pathology (8 decks)

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