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Soft Tissue Patholog
Week 4
| Question | Answer |
|---|---|
| List the 5 cardinal signs of inflammation | Heat (due to more blood flow in area after injury), redness, swelling (lots of fluid in injured area), pain (injury to nerve fibres) & loss of function |
| Without inflammation there is no...? | Swelling |
| Effect 1 of Inflammation: Primary Injury, what is it caused by? | Initial tissue disruption caused by: physical agents (force, burn), metabolic processes (schema & hypoxia), biological agents (bacteria, viruses) & chemical agents (acids & gases) |
| What is schema and hypoxia? | Ischemia: lack of blood flow Hypoxia: lack of oxygen |
| Effect 2 of Inflammation: Ultrastructural changes | 1. Breaking down & eventual disruption of the cellular membrane & its organelles. 2. The cells contents spill out of the extracellular space |
| Effect 3 of Inflammation: Chemical Mediation | Ultrastructural changes trigger the release of chemical mediators (histamine, bradykinin & prostaglandin) which signal the rest of the body that cells have been damaged. This mobilises the body's resources to respond. |
| Effect 4 of Inflammation: Hemodynamic Changes | Mobilize & transport defence components of the blood to the injury site. Secure their passage through vessel walls into the tissue. |
| Effect 5 of Inflammation: Metabolic Changes (8 steps) | Injury= cell hypoxia = switches to anaerobic metabolism = not long lasting = cell membrane function slows down = accumulation of Na+ ions in cell = causes cell to swell & burst = cell eventually dies |
| Effect 6 of Inflammation: Permeability Changes | Chemicals increase permeability of small blood vessels (histamine & bradilemen). Purpose of increased permeability is to let leucyotes move to the injury site |
| Effect 7 of Inflammation: Leucocyte (white blood cell) migration | Concentration limited migration: increased at sites where the greatest tissue damage has occurred. |
| List the 2 types of leucocytes and give 3 characteristics of each | Neutrophilis: smaller, faster, numerous. Temporary (7hrs) first line of defence does not reproduce. Macrophages: lives for months, can reproduce, cleaning up of cell debris |
| Effect 8 of Inflammation: ? | Phagocytosis |
| What is the difference b/w primary & secondary injury? | Primary injury occurs during initial result while secondary injury occurs gradually which is further tissue damage after primary injury. |
| List the 2 types of primary injury and what it is caused by | 1. Macrotrauma (impact/contact injury) caused by large insult & results in immediate tissue disruption. 2. Microtrauma (overuse or cyclic loading or friction injury) caused by small/low grade stress that wears away the tissue over time. |
| List & explain the 2 types of secondary injury | 1. Secondary enzymatic injury which involves the death of a cell from primary injury 2. Secondary metabolic injury which is prolong local ischemia caused by primary injury. It is the loss of balance b/w energy needed & energy available |
| Explain the difference b/w swelling and oedema | In swelling colour changes due to lots of debris/red blood cells while in oedema there is no change in colour & it can cause swelling |
| Define Swelling | Increase in tissue volume due to extra fluid & cellular material in tissue |
| Define oedema | Accumulation of the fluid portion of blood in tissue. Occurs hours after injury. |
| How does oedema result in the process of fluid exchange? | When more fluid moves out of the capillary and is then reabsorbed, oedema results. |
| Explain the concept of normal fluid exchange (3) | Fresh fluid goes into the body, used blood back to the heart. It is an alternate pathway for larger molecules through the lymphatic vessels. Amount of fluid moves outside capillary = amt moves inside capillary |
Created by:
meunid
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