Chronic inflammation

Question 1

Chronic Inflammation

Answer 1

• 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

Question 2

Causes

Answer 2

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)

Question 3

Morphology

Answer 3

• 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

Question 4

Comparing inflamm

Answer 4

Question 5

Inflammation

Answer 5

Question 6

Cells

Answer 6

from BM

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

Myeloid lineage

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

Question 7

Macrophage

Answer 7

Question 8

Macrophages

Answer 8

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

Question 9

Macrophage

Answer 9

abundant cytoplasm & vesicular, bean shaped nuclei

Question 10

Immunity

Answer 10

Question 11

Activate Macrophages

Answer 11

Question 12

Plasma Cells

Answer 12

Clock face

Coarse chromatin

Question 13

Immune Rxn Cells

Answer 13

IgE

eosinophils- IgE, parasitic infection

• major basic prot
• recruited by eotaxin
• allergic rxn

mast cells

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

Question 14

Mast Cells

Answer 14

Question 15

Eosinophils

Answer 15

Question 16

Granulomatous inflammation

Answer 16

• 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

Question 17

Cascerous necrois

Answer 17

Question 18

Epithelioid Histiocytes

Answer 18

Always around center of granuloma

look like a foot print

Activated macrophages resembling epithelial cells

Question 19

Foreign Body Granuloma

Answer 19

Form giant cells

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

this is cholesterol example

Question 20

Foreign Body Giant Cell lung

Answer 20

Question 21

Suture

Answer 21

Question 22

Immune Granuloma

Answer 22

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

Question 23

Caseating Granuloa TB

Answer 23

Question 24

Cat Scratch Disease

Answer 24

non caseating geographic stellate necrotizing granulomata

Question 25

Non caseating Non necrotizing Granuloma sarcoid

Answer 25

immune disease usually in african americans Cannot have TB!

Question 26

Specific Infections w/ granuloma

Answer 26

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

Question 27

Foreign Bodies w/ granuloma

Answer 27

Endogenous- keratin & uric acid crystals in gout Exogenous- silica, asbestos dust, talc, suture material, silicone, prostheses

Question 28

Further issues w/ granulomas

Answer 28

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

Question 29

Acute phase Response

Answer 29

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

Question 30

Acute Phase Response

Answer 30

Acute phase prot * c reactive prot * fibrinogen * serum amyloid A prot Leukocytosis * neutrophilia * eosinophilia * lymphocytosis Leukopenia

Question 31

Fever

Answer 31

* 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

Question 32

Increase pulse & BP, decrease sweating

Answer 32

ANS adrenergic effect

Question 33

Rigors, chills, anorexia, malaise, somnolence

Answer 33

actions of cytokines on brain

Question 34

Sepsis fromm organisms & LPS

Answer 34

increase iN TNF, IL-1 DIC, hypoglycemia, hypotensive shock

Question 35

Acute Phase Proteins

Answer 35

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

Question 36

CBC

Answer 36

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

Question 37

Leukopenia in infection

Answer 37

* decreased WBC * typhoid fever & viral infections, rickettsia, protozoal infections * due to sequestered lymphocyte in LN * overwhelming infection-- disseminated cancer, rampant TB & alcoholism

Question 38

Defective Inflamm

Answer 38

* 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