Flashcards in Acute and Chronic Inflammation II Deck (15):
What is the sequence of steps leading from vasodilation to acute inflammation?
Vasodilation brings increased blood flow and increased permeability. Transudate exits into the tissues. Exudate follows afterwards, containing proteins and cells. Inflammatory cells infiltrate the tissues.
Why do granulomas develop?
Granulomas are many macrophages that combine into one, single, multinucleated cell in an effort to engulf a larger organism. May also develop in necrosis. This is called granulomatous inflammation and is indicative of infection.
What are some examples of necrotic and non-necrotic granulotamous inflammation.
Necrotic - bacterial, parasitic, or fungal infections. Non-necrotic - inorganic metals or dust, foreign bodies, sarcoidosis, Crohn's disease
What is the definition of granulomatous inflammation?
A specific type of chronic inflammatory reaction characterized by modified macrophages, giant cells, lymphocytes, and occasional plasma cells. Initiated by infectious or non-infectious agents, occurs in the presence of poorly digestible irritants.
What sort of reactions do eosinophils participate in, what sort of chemotaxins do they follow, and what do their granules contain?
Eosinophils participate in immune reactions mediated by IgE (allergic) and parasitic infections. They follow chemotaxins known as eotaxins. Their granules contain "major basic protein" which is toxic to parasites.
What sorts of infections may cause an acute inflammatory response, and which may only cause a chronic inflammatory response?
Bacterial infections cause acute inflammatory responses (opsonizing process leading to phagocytosis by PMNs). Viruses, fungi, and parasites may only cause chronic responses (Virsuses - T cell response, parasites - IgE & eosinphils). Granulomatous inflammation may be caused by bacterial (e.g., TB) or fungal (e.g., hyphal) infections.
What are abscesses and empyemas and cellulitis?
Abscesses are "newly formed" spaces created by the accumulation of inflammatory cells. Empyemas are formed by the buildup of exudate in anatomical spaces or cavities. Cellulitis is the buildup of exudate in the layers of the skin, creating concern about how deep the buildup goes.
What is a highly damaging possible outcome of cellulitis?
If the cellulitis infection reaches the fascial plane, it can travel anywhere that plane goes. Can lead to major amputations.
What is an ulcer?
An ulcer is a local defect or excavation of the surface of an organ that is produced by sloughing of inflammatory necrotic tissue. Commonly occur in the mucosa of mouth, stomach, and intestines. Decubitus ulcers may develop on the lower back in bed-ridden patients.
What causes collateral damage from inflammation?
Damage to normal tissue nearby inflammatory processes may be damaged by the contents of the inflammatory cells. Neutrophils release enzymes to damage invading bacteria that also damage cells, inflammatory mediators such as ROS and nitric oxide may also damage healthy cells.
What are some examples of diseases that cause collateral damage?
Acute necrotizing bronchopneumonia may cause intense PMN reaction that destroys alveoli in the lungs. Rheumatoid arthritis is an autoimmune disease that causes chronic inflammation. Macrophages attack the cells of the joints.
What is the role and danger of the lymphatic system?
The lymphatic system drains fluids from the tissues. Nodes contain T and B cells where antigen presenting occurs. Many immune responses occur in the lymphatic system. However, if the cells of the lymph do not stop the infection it may also serve as a conduit for dissemination of injurious agents. Microorganisms that gain access to the blood stream cause sepsis (bacteremia, fungemia, viremia). "Disseminated infection".
What are the S/Sx of local infection and of systemic infection/sepsis?
Local = Redness, heat, swelling, pain, loss of function. Systemic = Sleepiness/grogginess, anorexia, fever, elevated WBC, altered BP (evaluate for hypotension - "septic shock")
What laboratory tests are appropriate to evaluate inflammation?
1 - Hematologic profile (esp. WBC) 2 - Acute Phase Reactants (C-reactive protein) 3 - DIC related markers (disseminated intravascular coagulation) 4 - Microbiology and Immunology Studies (Rapid ID, culture, serology) 5 - Immunoglobulin quantitation