6. inflammation Flashcards
inflammation is
response of vascularized tissue for cellular injury
2nd line defense
brings hosts defense cells and molecules to site of injury
aim of inflammation
Characteristics of inflammation
Occurs in tissues with a blood supply
Activated rapidly within seconds
Depends on the activity of both cellular and chemical components
Nonspecific
local manifestation
cardinal signs
exudate plus types 4
exudate is a fluid that leaks out of blood vessels and into surrounding tissues as a result of inflammation or injury.
Serous exudate: Serous exudate is a clear, watery fluid that contains few cells and little protein. It is typically produced in response to mild inflammation or injury and is often seen in conditions such as allergic reactions or burns.
Fibrinous exudate: Fibrinous exudate is a thick, sticky fluid that contains large amounts of fibrin, a protein that forms a mesh-like network. Fibrinous exudate is often seen in conditions such as pneumonia or pericarditis, and the fibrin network can sometimes lead to the formation of adhesions between tissues.
Purulent exudate: Purulent exudate, also known as pus, is a thick, yellowish fluid that contains large numbers of white blood cells (primarily neutrophils) and microorganisms. Purulent exudate is typically seen in bacterial infections and can be a sign of an abscess or other localized infection.
Hemorrhagic exudate: Hemorrhagic exudate is a fluid that contains red blood cells, often giving it a reddish or pinkish hue. Hemorrhagic exudate can be seen in conditions suchas vascular inflammation or trauma, and may indicate bleeding or damage to blood vessels.
Cardinal signs of inflammation plus why
- Rubor (redness)
- Tumor (swelling)
- Calor (heat)
- Dolor (pain)
- Functio laesa (loss of function)
systemic inflammation
Systemic changes associated with inflammation are collectively called acute phase response or systemic inflammatory response syndrome (SIRS)
Includes; fever, plasma protein (APR) and Leukocytosis
mechanism of development of fever
macrophages release IL-1 and TNF
these increase cyclooxygenase
PGE2 is produced
so fever
ESR used in inflammation why?
red blodd cells are negatively charged
during inflammation they are coated by coagulatiion factors which are produced in exccess
negative charge reduce so aggregation increases and repulsion decreases
so aggregated RBCs fall faster
ESD higher
difference between leukmoid reaction and chronic myelogenous leukemia
pic
systemic manifestation
leukocytosis
Increased pulse and blood pressure, rigors, chills, anorexia, somnolence and malaise
Weight loss
Reactive hyperplasia of the mononuclear phagocyte system
types of inflammation
acute and chronic
acute inflammation
Occurs within minutes of injury, lasts for hours or days and represents the early body reaction (part of innate immunity)
Characterized by neutrophils, fluid and plasma protein exudation
Stimuli for acute inflammation; Infections, Tissue necrosis, Trauma, Physical and chemical agents, Foreign bodies, Immune reactions
components of inflammation
Vascular response
Cellular response
Humoral response (chemical mediators)
for inflammatory reaction how is permeability increased
-Formation of endothelial gaps
(immediate transient response) - contraction by histamine and leukotryins- veins
-Direct endothelial injury
(immediate sustained response) - caused by burns or toxins - all vessels
-Delayed prolonged leakage- by uv rays or x rays - capillary and veins
-Leukocyte dependent injury- proteolytic enzymes eat the elastase- vein and glomerullar or pulmonary capillaries
-Increased transcytosis- VEGF affects the permeability of blood vessels by increasing the number and size of vesiculovacuolar organelles (VVOs). VVOs are interconnected channels made of vesicles and vacuoles that are found in the endothelial cells lining blood vessels.
-Leakage from new blood vessels
-
