Systemic Disease Flashcards
defense response that eliminates the products of cellular injuries (necrotic cells and debris), plays a role in the healing of injured cells by diluting or destroying the agent responsible for injury
inflammation
acute inflammation
an immediate response to injury that occurs 1-2 minutes post-injury, deterministic (happens the same way every time)
generates redness, heat, pain, swelling, and has presence of WBCs
3 major components of acute inflammation
- vascular size changes (dilation) to facilitate increased blood flow
- structural changes in the microvasculature (increased permeability) to facilitate the arrival of plasma proteins and leukocytes from the circulation
- immigration of neutrophils (PMNs) from circulation to the site of injury
outcomes of acute inflammation
complete resolution, scarring, fibrosis, abscess formation, and/or progressing to chronic inflammation
chronic inflammation
prolonged inflammation lasting from weeks to years. active inflammation, tissue injury, and healing all progress at the same rate
chronic inflammation is characterized by:
- infiltration with mononuclear cells (macrophages, lymphocytes, and plasma cells)
- tissue destruction
- repair involving new vessel proliferation (neovascularization) and fibrosis
chronic inflammations will arise in the following situations:
persistent infections, prolonged exposure to potentially toxic agents, and autoimmune diseases
major differences between chronic and acute inflammation
acute begins 1-2 minutes post-injury, chronic lasts weeks to years
acute involves PMNs and chronic involves macrophages, lymphocytes and plasma cells
acute happens the same way every time, chronic inflammation is not all the same, some types are granulomatous some are not
granulomatous inflammation
a type of chronic inflammation that is marked by large, activated macrophages with a squamous cell-like appearance
examples of granulomatous inflammatory diseases
bacterial - tuberculosis, leprosy (hansen), syphilis
fungal - histoplasmosis, blastomycosis
foreign body - suture, vascular graft
unknown - sarcoidosis
local factors that prolong wound healing
local infections, decreased blood supply, or the inability to form clots
systemic factors that prolong wound healing
immunocompromised states including diabetes, decreased peripheral blood flow, systemic infection, malnutrition, and increased glucocorticoid production (stress)
reversible cell injury
marked by a decrease in blood supply to a cell and a corresponding decrease in oxygen supply (hypoxia) will cause an increase in lactic acid concentration (decrease in tissue pH) and a decrease in ATP production (causes an accumulation of intracellular sodium and then cellular edema)
it is reversible when oxygen is restored to the cell and normal ATP, aerobic respiration, and sodium-potassium pump function is restored
irreversible cell injury
persistent ischemia and insufficient ATP results in sodium accumulation which causes edema in the cell disrupting the membrane and causing crucial components needed for ATP production to leak out (irreversible tissue necrosis)
irreversible tissue necrosis
progressive loss of membrane phospholipids, cytoskeletal abnormalities, toxic oxygen radicals which damage the cell membrane and other cell components, lipid breakdown products that accumulate in ischemic cells and result in phospholipid degradation
two processes occur with necrosis
- enzymatic digestion of the cell
- denaturation of proteins
four types of necrosis
coagulative, liquefactive, caseous, fat necrosis
apoptosis
well-organized self-destruction of cells (programmed cell death), critical in fine-tuning the developing retina!
coagulative necrosis
the structural boundary of a coagulated cell, tissue, or vessel is maintained, but integral structural proteins are denatured. occurs for example following a myocardial infarction
liquefactive necrosis
a cell with a well-defined boundary remains but consists of dull, gray-white remains. seen in fungal infections in the lungs
caseous necrosis
central necrotic tissue appears white and cheesy, example in tuberculosis infections
fat necrosis
death to adipose tissue, small white lesions are formed
Types of hypersensitivities
Type I - anaphylactic (first and fast)
Type II - cytotoxic
Type III - immune complex-mediated
Type IV - delayed or cell-mediated
Anaphylactic (Type I) hypersensitivity reaction
an allergen activates a B-lymphocyte and IgE antibodies are produced and bind to the surface of mast cells and basophils. A second exposure to the allergen causes cross-linking of IgE, allowing calcium to enter and resulting in degranulation of the cell. Histamine is the primary mediator released from the mast cells and basophils.
The initial response is 5-30 minutes and resolved in 30-60 minutes. Late phase response can be 4-6hours later