Wahedra2.txt

Card Set Information

Author:
emm64
ID:
120480
Filename:
Wahedra2.txt
Updated:
2011-12-03 18:39:08
Tags:
F2 Chronic
Folders:

Description:
F2 Chronic wahedra
Show Answers:

Home > Flashcards > Print Preview

The flashcards below were created by user emm64 on FreezingBlue Flashcards. What would you like to do?


  1. Acute V Chronic Inflammation
  2. Cellular Aspects of Chronic Inflammation
  3. chronic inflammation
    • If damaging stimulus persists the process of continuing tissue necrosis, organization, and repair all occur concurrently
    • -Infiltration with mononuclear cells
    • -Induced by persistent offending agent or by inflammatory cells
    • -Healing through connective tissue replacement of damaged tissue
    • -Accomplished through proliferation of small blood vessels (angiogenesis) and fibrosis
    • Tissue damage is a hallmark of chronic inflammation
  4. macrophage
    • most important cells involved in chronic inflammation
    • converted by inactive monocytes by the trophic signal, interferon gamma (produced at site of infection, then circulates in body)
    • -types of macrophage morphological changes:
    • 1)epitheloid cell- if there is a lot of cytoplasm
    • 2) multinucleated histiocytic giant cells- if there is fusion of many macrophages
    • Gain of function: phagocytic and secretory functions against injurious agents and for cell-mediated immunity (e.g. antigen presentation)
  5. Epithelioid cells
    • Activated macrophages with epithelial (squamous) cell like appearance
    • indistinct cell boundaries
    • abundant pale staining granular cytoplasm elongated/oval, slipper shapped nuclear
    • Weakly phagocytic
  6. Giant cells
    • When macrophages (epithelioid) cells fail, they fuse together to form multinucleated giant cells
    • 40-50 um
    • Weakly phagocytic
    • aka Langhan’s type, Touton giant cells, Aschoff cells
  7. Macrophage Secretions
    • Mediators of acute inflammation
    • -Platelet activator and arachidonic acid metabolites
    • Highly reactive oxygen metabolites
    • -Bacterial and cell killing
    • Proteases and hydrolytic enzymes
    • -Dissolution of extracellular matrix
    • Cytokines IL-1 and TNF-a
    • -Fibroblast proliferation and collagen synthesis—repair
    • Growth factors (PDGF, EGF, FGF)
    • -stimulate growth of blood vessels and division/migration of fibroblasts
  8. IFNgamma
    causes further differentiation in macrophages
  9. Activated Macrophage Diagram
  10. Lymphocytes
    Mobilization of antibody – mediated responses
  11. Mast Cells
    • Widely distributed in connective tissues and participate in both acute and persistent inflammatory reactions
    • Binds the Fc portion of the IgE antibody
  12. Plasma Cells
    Produce antibody directed either against persistent antigen in the inflammatory site or against altered tissue components
  13. Eosinophils
    • parasitic infections
    • Mediated by IgE
    • Eotaxin – a chemokine that has the ability to prime eosinophils for chemotaxis
  14. Acute V chronic Diagram
  15. Chronic Inflammation Facts
    • Predisposed by factors that prevent elimination of damaging stimulus
    • Tissue damage, acute inflammation, granulation tissue, repair, and immune reponse occur concurrently
    • Infiltration by lymphocytes demonstrates immune response in tissue
    • May develop after acute inflammation or may be a primary response to certain stimuli
    • Predisposing factors include persistent damaging stimulus, inadequate host response to infection and persistent autoimmune disease
  16. Chronic Histology
    necrotic cell debris, acute inflammatory exudate, vascular and fibrous granulation tissue, lymphoid cells, macrophages and collagenous scar
  17. impaired inflammation
    • 1) defective inflammation- chronic inflammatory response cannot be elicited, causing increased susceptibility, delayed wound healing, and tissue damage
    • 2) excess inflammation- seen in allergies, plays a role Cancer, Atherosclerosis, Autoimmune disease
    • Fibrosis as a sequel of chronic infections, metabolic conditions
  18. Unchecked substances that lead to tissue injury
    • Cause excess inflammation
    • Toxic O2 metabolites
    • Proteases
    • Neutrophil chemotactic factors
    • Coagulation factor
    • AA metabolites
    • Nitric oxide
  19. Unchecked substances that lead to Firosis
    • Growth factors
    • (PDGF, FGF, TGG-b)
    • Fibrogenic cytokines
    • Angiogenesis factors (FGF)
    • Remodelling collagenesis
  20. Chronic inflammation diseases
    • Chronic peptic ulcer
    • infections with persistent microbes
    • -tuberculosis
    • autoimmune disorders (RA, SLE)
    • prolonged exposure to toxic agents
    • (foreign body reactions)
  21. Chronic Peptic Ulcer
    • Protective mechanism of upper alimentary track breaks down
    • HCL and proteolytic enzymes destroy epithelium and supporting stroma  Acute inflammatory reaction
    • Acute inflammatory reaction occurs
    • -formation of exudate close to the acid exposed surfaces while in the depths of the ulcer (farthest from the acid) attempts are made to organize the exudate and granulation tissue forms  Collagenous scar
    • Ulceration of the wall stomach or duodenum persistent damage
  22. ulcer
    • local defect, or excavation, of the surface of an organ or tissue that is produced by the sloughing(shedding) of inflammatory necrotic tissue
  23. Granulomatous Inflammation
    • Cellular attempt to contain an offending agent that is difficult to eradicate.
    • In this attempt there is often strong activation of T lymphocytes leading to macrophage activation, which can cause injury to normal tissues.
    • Distinctive pattern of chronic inflammation that is encountered in a limited number of infectious and some noninfectious conditions.
    • Recognition important in the clinic: limited number of possible conditions that cause it and the significance of the diagnoses associated with the lesions
  24. Granuloma
    • discrete clusters of macrophages and lymphocytes
    • Macrophages develop an epithelial-like (epithelioid) appearance (GRANULOMA)
    • In time develops an enclosing rim of fibroblasts and connective tissue (Fibrosis)
  25. Immune granulomas
    • Caused by insoluble particles that are capable of inducing a cell-mediated immune response
    • Macrophages are transformed into Epitheloid cells and multinucleate giant cells
    • Examples:
    • Bacteria
    • Tuberculosis *** (high incidence due to drug resistant stains)
    • Leprosy
    • Parasites
    • Schistosomiasis (3 types)
    • Fungi
    • Histoplasmosis
  26. 2.Foreign Body Granulomas
    • Don’t incite either an inflammatory or immune response.
    • Epitheloid cells and giant cells are apposed to the surface and encompass the foreign body.
    • The foreign body is usually found in the center of the granuloma.
    • Examples:
    • Metal/Dust
    • Berylliosis
    • Silicosis
    • Foreign body
    • Splinter
    • Suture
  27. Sarcoidosis
    • granulomatous inflammation
    • Bad systemic disease, probably autoimmune disease
    • Etiologic agent is unknown
  28. Granuloma histological example
    • Caseous necrosis at center
    • Macrophages and epithelioid cells
    • Lymphocytes & plasma cells- form a ring
    • Giant cell
    • Arrow: fibrosis
  29. Tuberculous granuloma
    • Central necrosis surrounded by a collection of large, activated macrophages that have some resemblance to epithelial cells; “epithelioid” cells
    • Langhan's giant cells
    • Outside and around the macrophages is a collar border of lymphocytes
    • Over time, some fibroblasts appear in the lymphocytic collar (macrophage cytokine recruitment)
  30. Langhan’s giant cells
    • activated macrophages that fuse to form large, multinucleated cells.
    • Many nuclei around the periphery and a large central cytoplamic mass

What would you like to do?

Home > Flashcards > Print Preview