Pathology cptr2 ( acute & chronic inflammation)
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Pathology cptr2 ( acute & chronic inflammation)
- 3. 2) (Rote?) Learn the roles of various “chemical mediators” of acute inflammation 3) Know the three possible outcomes of acute inflammation 4) Visualize the three morphologic patterns of acute inflammation 5) Understand the causes, morphologic patterns, principle cells, minor cells, of chronic and granulomatous inflammation
- 7. ACUTE INFLAMMATION Neutrophil Polymorphonuclear Leukocyte, PMN, PML “ Leukocyte” Granulocyte, Neutrophilic granulocyte “ Poly-” Polymorph
- 8. Rubor Calor Tumor Dolor 5 th (functio laesa) HISTORICAL HIGHLIGHTS (Egypt, 3000 BC)
- 12. LEAKAGE OF PROTEINACEOUS FLUID ( EXUDATE , NOT TRANSUDATE)
- 39. BLISTER, “Watery”, i.e., SEROUS
- 40. FIBRINOUS
- 41. PUS = PURULENT ABSCESS = POCKET OF PUS
- 43. ULCERATIVE
- 45. CHRONIC INFLAMMATION (MONOS) LYMPHOCYTE MONOCYTE MACROPHAGE HISTIOCYTE
- 49. GRANULOMAS GRANULOMATOUS INFLAMMATION 4 COMPONENTS FIBROBLASTS LYMPHS HISTIOS “ GIANT” CELLS
- 50. GRANULOMAS GRANULOMATOUS INFLAMMATION CASEATING (TB) NON-CASEATING
- 53. NORMAL SPE Serum Protein Electrophoresis In ACUTE Inflammation Alpha-1 & alpha-2 are increased, i.e., “ acute phase” reactants.
Editor's Notes
- Think of it as a Cecil B. DeMille epic movie!
- The sequence of changes occurring in acute inflammation are NOT specific for the stimuli which cause them
- These are the three “phases”, in order, of acute inflammation. Please NOTE they, in no way, are the independent of each other, and as you might suspect by now, quite the contrary, CRUCIALLY all wrapped up with each other!
- Many names, same cell
- The four “cardinal”, i.e., “classic” signs of inflammation, translated, literally, 1) redness, 2) heat, 3) swelling, 4) pain. Just like a fith Marx bother, Gummo, was often added, so was the term “functio laesa” or “loss of function”
- The usual suspects, again. “Stimuli”, like “etiologic agents” is a very elusive term if you like to think in terms of ultimate causes.
- Vascular changes occur BEFORE any infiltration of inflammatory cells arrive.
- These are all events which either cause, or result, from the phenomenon of “increased permeability”
- Transudate vs. Exudate. Transudates can be thought of as being fairly pure water. Transudates are water PLUS most serum proteins, fibrin, and many blood cells often.
- The four things neutrophils do, in order, in acute inflammation.
- Secretins and integrins are classes of substances to help neutrophils stick to vessel walls and migrate through the wall.
- Chemokines
- These three events are the results of leukocytes (i.e., neutrophils) being “activated”
- The three phases of phagocytosis, in correct order.
- These are the common features of ALL “chemical mediators” in acute inflammation.
- How many of the 4 cardinal signs of inflammation can histamine cause, by virtue of its being a powerful vasodilator?
- Serotonin is widely and primarily thought as being a neurotransmitter involved in the full spectrum of emotional responses, but its role in acute inflammation is just as powerful.
- Complement fixation id the end stage of a cascade of multiple chemical events, similar to coagulation, which ultimately result in lysis of cell membranes, hopefully, bad cells.
- Bradykinin is a potent endothelium -dependent vasodilator , causes contraction of non-vascular smooth muscle , increases vascular permeability and also is involved in the mechanism of pain .
- Coagulation is also a cascade, like complement fixation.
- Hypercoagulability is anything which accelerates the cascade, or inhibits its inhibitors
- Three classic eicosanoids, new classes are also being discovered. ALL are derivatives from arachidonic acid.
- Arachidonic acid
- When you think of the three main things that ASPIRIN does, you can remember the three main properties of the prostaglandins.
- Click back to the previous slide on LEOKITRIENES and realize that LIPOXINS generally do the OPPOSITE of what LEUKOTRIENES do.
- It is produced in response to specific stimuli by a variety of cell types, including neutrophils , basophils , platelets , and endothelial cells .
- There are gazillions of cytokines/chemokines. The two most classical and famous ones are TNF-alpha and Interleukin-1. TNF, also called tumor necrosis factor, or cachectin, is a substance that is destructive of human tissues, and is a key player in “cachexia”. Interleukin-1 was the first of many interleukins discovered and generally propagates the inflammatory response at many levels and also has a significant effect on T-cells.
- Which drug INCREASES the effect of nitric oxide? Hint: you get spam ads for it 10 times a day in your spam, even if you are a female.
- MPO produces Hypochlorous acid and tyrosyl radical are cytotoxic , so they are used by the neutrophil to kill bacteria and other pathogens . It is what makes pus look greenish yellow. Lactoferrin (LF), also known as lactotransferrin (LTF), is a globular multifunctional protein with antimicrobial activity ( bacteriocide , fungicide ) Lysozymes , also known as muramidase or N-acetylmuramide glycanhydrolase , are a family of enzymes ( EC 3.2.1.17 ) which damage bacterial cell walls by causing hydrolysis .
- Substance P is an 11 amino acid polypeptide tied into many things including mood disorders, anxiety, stress, reinforcement, respiration rate, neurotoxicity, nausea, emesis, and pain. The Neurokinins are also peptide neurotransmitters involved in many things.
- Three classic outcomes of acute inflammation
- I must have said THREE patterns, but this looks like four to me. Who cares? Remember, they are only adjectives! (Onelook.com has 133 adjectives to the word “inflammation”)
- FINRIN is the endpoint of coagulation and had a characteristic appearance both grossly and microscopically. Do you remember hearing the term fibrin-OID necrosis too?
- It is EXTREMELY important to be able to recognize neutrophils (Polys) in H&E sections. The key tip is, OFTEN, they might NOT look multilobulated at first, but upon close examination, they are!
- ULCERS (i.e., pathologic LOSS of mucosal or epithelial coverings, are both the CAUSE as well as a RESULT of acute inflammation. WHY? Identify the FOUT layers of the colon here, mucosa, submucosa, muscularis, and finally adventitia/serosa.
- What does chronic inflammation look like? ANS: Infiltrates of lymphs and monos “peppering” normal histology.
- Please note that the “cellular” players of chronic inflammation are NOT the baseball players who play in US Cellular Field in Chicago, i.e., the White Sox.
- The drainage patters of acute or chronic inflammation follow the same general drainage patterns of tumor cells.
- CRP is a member of the class of acute phase reactants as its levels rise dramatically during inflammatory processes occurring in the body. It is thought to assist in complement binding to foreign and damaged cells and affect the humoral response to disease. It is also believed to play an important role in innate immunity, as an early defense system against infections.
- Which TWO of these 5 “hills” are significantly higher in nonspecific systemic acute inflammation? Answer: alpha-1 and alpha-2