(06) LEcture 6 Flashcards
(Granulomatous Inflammation)
- chronic or acute process?
- What is the main componenet?
- Usually associated with what?
- chronic
- macrophages
(Granulomatours Inflammation)
- Th1-based granulomas = ?
(Immune Response: T helper cells (CD4) plus cytotoxic T cell (CD8))
- Th1 - favor what kind of immune response?
- Th1 cells produce IL-2 which starts a sequence - what is it?
(can react to exogenous or endogenous (auto-immune))
- classic “tuberculoid” type
- cell mediated (in response to IL-12, IFN-y, and others)
- IL-2 –> t lymphocyte proliferation –> IFN-y and TNF-b –> activation of mo and DC
(Chronic Inflammation)
(Immune Response: T helper cells (CD4))
- Th2 - favor what kind of immune response?
- Th2 cells produce IL-4, IL-5, IL-10 which cause what to happen?
- allergies
- often attract what other two cells?
- Th2 biased granuloma –> what type?
- humoral (in response to IL-4 and IL-10)
- IL-4, IL-5, IL-10 –> B lymphocyte proliferation and plasma cell differentiation (–> plasma cell rich infiltrates)
- mast cells and eosinophils
(Granulomatous Inflammation)
(Causes)
1-2. give me the two
- endogenous (keratin, cholesterol, urates, etc) or foreign material (asbestos, silicates, suture material, plant material) to is resilient to degradation by macrophages
(Granulomatous inflammation)
(Foreign body type granuloma - low turnover)
- Inciting cause without what and what?
- is there a negative result for host organism?
(Foreign Body Type granuloma - high turnover)
- inciting cause without what but with what?
- harmful to host?
- proliferative an aggressive capacity (suture material)
- no
- without proliferative capacity but with aggressive capacity (urates, asbestos)
- after a (often long) period of time
(Granulomatous Inflammation)
(foreign body type granuloma)
- what does gross lesion look like?
- What do you see in histology?
- “quiet beige” - usually well demarcated (tumor-like)
(Granulomatous INflammation)
(Epitheloid Cell Granuloma (lepromatous type/histiocytic inflammation)
- proliferating? aggressive?
- how is immune response?
- What do you see grossly?
- What do you see in histology?
- necrosis? layered appearance?
- yes; no
- good
- gradual replacement (chronic progressive) of organ by poorly defined beige firm tissue (infiltrative) –> impairment of organ function
- large numbers of epitheolid macrophages (+/- lymphocytes and plasma cells)
- no, no
(Granulamatous Inflammation)
(Classic granuloma - tuberculoid type)
- proliferating? aggressive?
2-4. Course is dependent on what three things?
- yes, yes (mycobacterium tuberculosis)
- interplay of proliferative and aggressive interplay of infectious agent
- immune condition of host
4.
(Granulomatous Inflammation)
(Classic Granuloma - tuberculoid type)
- layered appearance of granuloma?
- with or without caseous necrosis?
- what two cell types in interface?
- What 3 cells in periphery?
- What happens to lesion and agent if immune system is “good”?
- What occurs if immune system is weak?
- yes
- can be either
- epitheloid macrophages and langhans type multinucleated giant cells
- lymphocytes, plasma cells, and fibroblasts
- is contained
- overwhelming proliferation of agents with widespred necrosis and poor cellular response
(Granulomatous Inflammation)
(Lymphoplasmacytic Inflammation)
- detectable grossly?
- Histological: frequently as what?
3-5. Plasma cell rich infiltrates: seen in what three things?
- often not
- perivascular infiltrates
(Lymphoplasmacytic Inflammation)
1-3. Difficult to Distinguish from what three things?
- lymphoid tissue of juvenile animals
- regular immune function in tubular organs (lympho-follicular inflammation)
- chronic suppurative inflammation in tubular organs
(this slide was in this section - but I don’t really know if it belongs under this type of inlammation or not)
(Eosinophils in Inflammation)
(Etiology - study of causation… why can’t i remember this…)
1-5. what are five causes?
- parasite infection
- IgE mediated hypersensitives
- paraneoplastic syndromes (mast cell tumor, lymphoma)
- Hypereosinophilic syndroms
- animal species (pig, raccoon, others?) (?)
(Erosive and Ulcerative Inflammatino)
- Type of inflammation of what two things?
- What is a defect of multi-layered epithelium that does not extend beyond stratum basale/basement membrane?
- 1 What do you see grossly? distinguishable from superficial ulcer?
- Histology: basement membrane intact? Only mild inflammatory reaction in what?
- skin and mucous membranes
- erosion
- 1 slight depreesion (theoretically); no
- 2 yes
(Erosive and Ulcertaive Inflammation)
(Erosion)
- Due to what?
- ruptured vesicle (eg after viral infection and burns)
(Erosive and ulcerative inflammatin)
- What is a defect that extnds beyond stratum basale/basement membrane with ulcer margins and ulcer base?
- What do you see grossly? Is there any bleeding? bordered by raised rim of granulation tissue when what?
- ulcer
- slight (superfical ucler) to deep depression (deep ulcer)
may see bleeding at base due to destruction of blood vessels in subcuti/lamina propria mucosase
(Erosive and Ulcerative Inflammatin)
(ulcer)
(Histology)
- basement membrance intact?
- mild to marked inflammation in what?
- granulation tissue?
(Sequela)
- tends to become chronic with what?
- may do what if it gets bad enough?
- no (it is disrupted/destoyed)
- subcutis/lamina propria
- in chronic cases
- chronic hemorrhage (–> anemia)
- perforate (mainly in stomach –> peritonitis)
(Papular/proliferative inflammation)
- what is hyperplasia of epithelial cells as principle response to a viral infection (eg poxvirus or parapoxvirus)?
- Macule –> papule (–> vesicle –> pustule –> ulcer or crust/scab) (?)
- Proliferative lesions of the epidermis are also common with what?
- papule
