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Pathology 2-1
Duke PA pathology
| Question | Answer |
|---|---|
| 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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