0.2 Tissue response to Injury Flashcards
What is necrosis?
Evidence of cell death in a living body
Callular leakage leading to inflammation which removes cellular debris
What is coagulative necrosis associated with?
Ischemia (reduced blood flow / lack of oxygen)
Pyknosis, Karyorrhexis, and Karyolysis
What is liquefactive necrosis associated with?
Related to microbial growth
Tissue transformed into liquid / viscous mass (microbes eat biological tissue turning stucture into liquid / pus)
What is caseous necrosis associated with and how does it visually appear macroscopically and microscopically?
Specific to TB, syphilis, and some fungi
Macroscopically = cheesy tan/white
Microscopically = pink, proteinaceous mass encapsulated by granulomatous processes
What is apoptosis?
Programmed cell death
No cell leakage, no inflammation
What is acute inflammation?
Coordinated host response to injury
Preprogrammed = similar for all causes
Mostly vascular and local changes
What is chronic inflammation?
Next progression, if acute inflammation is unable to deal with bacterial load
Long standing response to long standing injury in which injury and repair occur simultaneously
Different patterns depending on case, but feature emigration of monocytes/lymphocytes into tissues
Wound healing can be undertaken by regeneration or repair. What is the difference between them?
Regeneration = replacement of tissue with original tissue eg liver
Repair = blood clot or nectrotic tissue replaced with granulation tissue (matures to scar/bone/adipose)
What are the two types of immunity?
- Non-specific / innate
- Specific / adaptive
What are the characteristics of non-specific / innate immunity?
- Not targeted to specific organsims
- Does not increase after first exposure to organism
What are the characteristics of specific / adaptive immunity?
- Targeted to specific organisms
- Increases following exposure
- Confers future protection against organism
What are the four classical signs of acute inflammation?
- Swelling
- Pain
- Redness
- Heat
The major changes for acute inflammation are vascular to better get blood into tissues with leukocytes and plasma protective factors. How do these changes relate to the classical signs of acute inflammation?
- Vascular leakage = swelling
- Limited movement = pain
- Vasodilation = Redness + heat
What are the 3 morphological types of acute inflammation?
- Suppurative = pus formation
- Serous = voluminous clear fluid produced
- Fibrinous = fibrin deposited on a surface
Opening of vasculature brings blood to the body surface, which is normally cooler than the core temperature, resulting in redness and heat. What are the steps behind vascular dilation?
- Increased blood flow = arteriole + venule dilation and the expansion of capillary bed
- Leads to edema = swelling + leakage of plasma/proteins in ECM
- Neutrophils emigrate into EM (normally only occasional lymphocytes + macrophages)
What are Starling’s forces?
Relationship between hydrostatic and oncotic pressure
What is the process behind vascular leakage?
Inflammatory mediators increase endothelial permeability
Protein leaks out, water follows = protein rich exudate / inflammatory oedema
Swelling in acute inflammation is caused by increased vascular permeability and vascular leakage. Starling’s forces play a key role in this. Explain how.
- Net Flow shifts from normal to outward via increased hydrostatic pressure
- Vessel dilates to accomodate pressure changes
- Pressure changes allow plasma proteins + water to leak out in rich exudate (oedema)
Oedema plays an important role in acute inflammation. What is it?
- Oedema dilutes toxins and increases lymph flow
- Lymph flow takes toxins / bacterial products out of area
- Bacterial antigens + toxins presented to lymph nodes for development of immune response