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