Path - Inflammation (Inflammation, Chromatolysis, Calcification, & Leukocyte extravasation) Flashcards
Pg. 223-224 in First Aid 2014 Sections include: -Inflammation -Chromatolysis -Types of calcification -Leukocyte extravasation
What are the 5 main findings/factors that characterize inflammation?
Characterized by (1) Rubor (redness) (2) Dolor (pain) (3) Calor (heat) (4) Tumor (swelling) (5) Functio laesa (loss of function)
What does the vascular component of inflammation include?
Increased vascular permeability, vasodilation, endothelial injury
In general, what cells and processes does the cellular component of inflammation involve?
Neutrophils extravasate from circulation to injured tissue to participate in inflammation through phagocytosis, degranulation, and inflammatory mediator release
What are the 3 mediators of acute inflammation?
Neutrophil, eosinophil, and antibody mediated
What are the 2 mediators of chronic inflammation?
Mononuclear cell and fibroblast mediated
What is the onset and time course of acute inflammation?
Acute inflammation is rapid onset (seconds to minutes), lasts minutes to days.
What are 3 potential outcomes of acute inflammation?
Outcomes include complete resolution, abscess formation, and progression to chronic inflammation
What 2 events/processes characterize chronic inflammation?
Characterized by persistent destruction and repair
With what 2 processes is chronic inflammation associated?
Associated with blood vessel proliferation, fibrosis
With what type of inflammation does granuloma occur? What is a granuloma?
Chronic inflammation; Granuloma: nodular collections of epithelioid macrophages and giant cells
What are 2 outcomes of chronic inflammation?
Outcomes include scarring and amyloidosis
What is Chromatolysis?
Process involving the cell body following axonal injury
What do the changes seen in Chromatolysis reflect, and why?
Changes reflect increased protein synthesis in effort to repair the damaged axon
What are 3 histological characteristics of Chromatolysis?
Characterized by: (1) Round cellular swelling (2) Displacement of the nucleus to the periphery (3) Dispersion of Nissl substance throughout cytoplasm
What are the types of calcification?
(1) Dystrophic calcification (2) Metastatic calcification
What is dystrophic calcification, and what causes it?
Calcium deposition in tissues secondary to necrosis
What is metastatic calcification, and what causes it?
Widespread (i.e., diffuse, metastatic) deposition of calcium in normal tissue secondary to hypercalcemia (e.g., primary hyperparathyroidism, sarcoidosis, hypervitaminosis D) or high calcium-phosphate product (e.g., chronic renal failure + secondary hyperparathyroidism, long-term dialysis, calciphylaxis, warfarin)
Again, what are the causes of metastatic calcification? Give at least 3 examples of each.
(1) hypercalcemia (e.g., primary hyperparathyroidism, sarcoidosis, hypervitaminosis D) or (2) high calcium-phosphate product (e.g., chronic renal failure + secondary hyperparathyroidism, long-term dialysis, calciphylaxis, warfarin)
What tends to be the extent of dystrophic calcification? Give an example.
Tends to be localized (e.g., on heart valves)
What are 9 conditions/findings in which dystrophic calcification is seen?
Seen in (1) TB (lungs and pericardium) (2) liquefactive necrosis of chronic abscesses (3) fat necrosis (4) infarcts (5) thrombi (6) schistosomiasis (7) Monckeberg arteriolosclerosis (8) congenital CMV + toxoplasmosis (9) psammoma bodies
What are the calcium findings in patients with dystrophic calcification versus metastatic calcification?
DYSTROPHIC CALCIFICATION: It is not directly associated with hypercalcemia (i.e., patients are usually NORMOCALCEMIC); METASTATIC CALCIFICATION: Patients are usuallly NOT NORMALCALCEMIC.
In metastatic calcification, in what tissues do calcium deposits predominate, and why?
Calcium deposits predominantly in interstitial tissues of kidney, lungs, and gastric mucosa (these tissues loose acid quickly; increased pH favors deposition).
Where does leukocyte extravasation predominately occur?
Extravasation predominantly occurs at postcapillary venules
Give the goal and big picture of Leukocyte extravasation without going into the details of each step.
Leukocytes exit from blood vessels at sites of tissue injury and inflammation in 4 steps: (1) Margination and rolling (2) Tight-binding (3) Diapedesis (4) Migration
What factors mediate margination and rolling in the vasculature/stroma versus leukocyte? Give 3 binding options (with numbers indicating what on the vasculature/stroma binds what on the leukocyte).
VASCULATURE/STROMA: (1) E-selectin (2) P-selection (3) GlyCAM-1, CD34; LEUKOCYTE: (1) Sialyl-Lewis X (2) Sialyl-Lewis X (3) L-selectin
What factors mediate tight-binding in the vasculature/stroma versus leukocyte? Give 2 binding options (with numbers indicating what on the vasculature/stroma binds what on the leukocyte).
VASCULATURE/STROMA: (1) ICAM-1 (CD54) (2) V-CAM-1 (CD106); LEUKOCYTE: (1) CD11/18 integrins (LFA-1, Mac-1) (2) VLA-4 integrin
What factor mediates diapedesis in the vasculature/stroma versus leukocyte?
VASCULATURE/STROMA: PECAM-1 (CD31); LEUKOCYTE: PECAM-1 (CD31) (i.e., same for both)
What occurs during diapedesis?
Diapedesis - Leukocyte travels between endothelial cells and exists blood vessel
What occurs during migration?
Migration - Leukocyte travels through interstitium to site of injury or infection guided by chemotactic signals
In general, what are the vasculature/stroma mediators for leukocyte migration? In response to what are they released? Give 5 examples.
Chemotactic products released in response to bacteria: (1) C5a (2) IL-8 (3) LTB4 (4) kallikrein (5) platelet-activating factor
What should you know about the leukocyte mediators of migration?
Various :-)
Draw a visual depicting leukocyte extravasation, numbering the steps and labeling key mediators.
See p. 224 in First Aid 2014 for visual
