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Pathology 2-1

Duke PA pathology

Inflammation response to injury
Reaction of blood vessels leads to accumulation of fluid and leukocytes in extravascular tissues
What does inflammation do to the injurious agent? destroys, dilutes, or walls off the injurious agent
What does inflammation do in the repair process? initiates it
itis inflammation
Is inflmmation protective or harmful? fundamentally protective, may be harmful
Examples of harmful inflmmation arthritis, atherosclerosis, scars, insect bites
What are the components of inflammatory response? vascular reaction, cellular (exudative) reaction
How is inflammation mediated? chemical mediators - derived from plasma proteins and from cells inside and outside of blood vessels
acute inflammation short duration, edema, and mainly neutrophils
chronic inflammation longer duration, lymphocytes & macrophage predominate fibrosis, new blood vessels (angiogenesis)
granulomatous inflammation distinctive pattern of chronic inflammation; activated macrophages (epithelioid cells) predominate
cellulitis inflammation of soft tissue - mononuclear cells predominate
rubor erythema (redness) - vasodilation, increased blood flow
tumor swelling - extravascular accumulation of fluid
calor heat - vasodilatation, increased blood flow
dolor pain
5th sign (Virchow) functio laesa - loss of function
What are the three major components of acute inflammation? increased blood flow, edema, leukocytes
What visible signs does increased blood flow cause? redness and warmth
In acute inflammation, what does edema result from? increased hydrostatic pressure (vasodilation) and lowered intravascular osmotic pressure (protein leakage)
What do leukocytes do in acute inflammation? emigrate from microcirculation and accumulate in the focus of injury
acute inflammation stimuli infections, trauma, physical or chemical agents, foregin bodies, immune reactions
During acute inflammation, increased hydrostatic pressure increases flow through lymphatics, causing what? increases antigen presentation and immune responses - lymph fluid enters back at thoracic duct
What effect does fluid accumulation have on toxins? dilutes toxins
How does fluid accumulation causing pain benefit the injury site? decrease use and prevent additional injury
Fluid accumulation cause rise in antibodies in blood which provide what benefit? can kill microbes
What can blood plasma proteins do to help in injury? amplify responses against the injurious agent
What is the first mechanism of increased vascular permeability? gaps due to endothelial contraction - fast and short lived (minutes, most common, venules
What is the second mechanism of increased vascular permeability? direct injury - toxins, burns, chemicals, fast and may be long lived - arterioles, capillaries, venules
What is the third mechanisms of increased vascular permeability? leukocyte-dependent injury - mostly venules, pulmonary capillaries, late response, long lived
What is the fourth mechanism of increased vascular permeability? increased transcytosis - venules, vascular endothelium-derived growth factor
What is the fifth mechanism of increased vascular permability? new blood vessel formation - angiogenesis - persists until intercellular junctions form
Extravasation delivery of leukocytes from the vessel lumen to the interstitium
What happens in the lumen in extravasation? margination, rolling and adhesion
diapedesis migration across the endothelium
chemotaxis migration in the interstitial tissue
What do leukocytes do in extravasation? phagocytize, kills microbes, degrade necrotic tissue and foreign antigens
What determines leukocyte adhesion and migration across vessel wall? binding of complementary adhesion molecules on the leukocyte and endothelial surfaces
What is the sequence of leukocyte emigration? neutrophils (6-24 hrs), monocyts in 24-48 hrs
What happens after neutrophils and monocytes show up in leukocyte emigration? induction/activation of different adhesion molecule pairs and specific chemotactic factors in different phases of inflammation
What do chemical mediators do in leukocyte adhesion? affect these processes by modulating the expression or avidity of the adhesion molecule
serous inflammation outpouring of thin fluid (serous effusion, blisters)
Fibrinous inflammation body cavities; leakge of fibrin; may lead to scar tissues
suppurative (purulent) inflammation pus or purulent exudate (neutrophils, debris, edema fluid) abscess: localized collections of pus
ulcers local defect of the surface of an organ or tissue produced by the sloughing of inflammatory necrotic tissue
chronic inflammation inflammation of prolonged duration (weeks or months)
What proceed simultaneously in chronic inflammation? active inflammation, tissue destruction, and attemps at repair
How does the timing of chronic inflammation intersect with that of acute inflammation? may follow acute inflammation or being insidiously and often asymptomatically
persistent infections Treponema pallidum (syphilis), viruses, fungi, parasites
Created by: ges13
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