L3 Inflammation Flashcards
acute inflammation
hours to weeks rapid onset neutrophil driven prominent vascular response innate immunity immediate reaction to tissue injury
chronic inflammation
persistent reaction to tissue injury slow response less prominent vascular response duration weeks to years cell-mediated immunity mononuclear cell predominance (lymphocytes, plasma cells, and monocytes)
acute inflammation causes
microbial infection, tissue necrosis, physical agents, chemical irritants, immune mediated hypersensitivity
chronic inflammation cuases
foreign body, autoimmune disorders, persistent tissue injury and acute inflammation, primary granulomatous disease, and microorganisms resistant to phagocytosis or intracellular killing (mycobacteria, viruses, fungi and some parasites)
inflammation is usually beneficial but it can definitely cause morbidity and mortality example being
fatal acute pneumonia
cardinal signs of inflammation
rudor - redness tumor - swelling dolor - pain calor - heat functio laesa - loss of function
vasoactive mediators of edema can be _________ and _______ derived and work to increase membrane permeability and increase vasodilation
cell or plasma
cell derived vasoactice mediators
- mast cells- histamine
- platelet cells - serotonin
- epithelium - nitric oxide, prostaglandins, platelet activating factor
- inflammatory cells- prostaglandins, platelet activating factor, and leukotrienes
plasma derived vasoactive mediators
- hageman factor activation- 1. kallikrein kinin system (KK cells) - kinin (bradykinin) 2. clotting/fibrinolytic system- fibrin split products
- complement system activation
inflammatory mediators
vasoactive mediators (leading to edema) and chemotactic factors (leading to acute and or chronic inflammation)
mechanisms of phagocytosis and cell killing
- C3b receptor and Fc receptor attach to antigens on bacteria
- respiratory burst
oxidative burst- order of events
1.
- molecular oxygen reduced by NADPH oxidase produces superoxide anion (o2) enzyme NADPHA oxidase
oxidative burst- order of events
2.
- generation of hydrogen peroxide enzyme superoxiide dismutase
oxidative burst- order of events
3.
- hydroxyl radical (OH) attacks DNA
oxidative burst- order of events
4.
- hypochlorous acid (HOCL) has many toxic effects
enzyme myeloperoxidase
chronic granulomatous disease
inherited disorder of phagocytic cells, results from an inability of phagocytes to produce bactericidal superoxide anions because lack NADPH oxidase, cannot break down bacteria because cannot form needed h2o2 and superoxide
aphagocytic cells are unable/able to kill catalase positive microorganisms because they can/cannot break down hydrogen peroxide
unable; can
catalase negative microorganisms can/cannot be killed in people with chronic granulomatous disease
can because they produce H2O2
migration out of vessels
macrophages send chemokines to inflame the blood vessel near the region of infection causing inflammatory cells to leave the blood vessel
fibrinous exudate
full of fibrin and edema fluid
fibrosis
end product of inflammation, scar tissue has not healed properly, fibroblast have laid down collagen
granulation tissue
end product of inflammation where the developing wound healing and repair, rebuilding new capillaries
granulomatous inflammation
specialized form of chronic inflammation where your body cannot get rid of the infection/organism/substance so forms a dense accumulation mononuclear phagocytes surrounded by a collar of lymphocytes
What is not considered a purpose or role of inflammation? generate inflammatory mediators localize/eliminate pathogenic insult promote local tissue damage repair injured tissue compartment restore normal physiology
promote local tissue damage
When compared to monocytes/macrophages, which is the most appropriate statement to describe neutrophils?
are longer lived
controls Mycobacterium tuberculosis
communicates with T-cells
antigen-presenting cell with MHC class II receptors
first to extravascular space in response to infection
first to extravascular space in response to infection
In oxygen-dependent killing of neutrophils, superoxide anion and hydrogen peroxide, respectively, are generated by which enzymes for the respiratory burst?
catalase and lysozyme
glutathione peroxidase and sulfhydryl oxidase
lactoferrin and gelatinase
myeloperoxidase and flavin reductase
NADPH oxidase and superoxide dismutase
NADPH oxidase and superoxide dismutase
Q1. Which of the following cytokines are most likely involved in the early stages of acute inflammation?
IL-4, IL-5, IL-13
IL-1, TNF-alpha, IL-6
Interferon beta & gamma
Terminal complement proteins
Cytokines are only involved in chronic inflammation
IL-1, TNF-alpha, IL-6
Q2. The physician seeing the child is concerned of a developing abscess. If an aspirate (with a needle and syringe) is obtained from the area of swelling, the inflammatory cells likely to be present in greatest numbers are: Mononuclear cells Dendritic cells B (Antibody producing) Cell Basophils Neutrophils
Neutrophils
Q3. Signs that this process was progressing to chronic inflammation would be:
Decrease in collagen (extracellular matrix)
Increase in arteriolar dilation
Increase in monocytes
Increase in histamine
This process can not progress to chronic inflammation
Increase in monocytes
Q5. CJ who has Chronic Granulomatous Disease (CGD) is not at increased risk of serious infections due to Streptococcus pneumoniae (in contrast to Staphylococcus aureus, Aspergillus, and select other organisms). Why?
S. pneumoniae is a catalase-negative organism which can produce hydrogen peroxide
Streptococci are not affected by oxygen radicals
The structure of the thin cell wall and outer membrane make it more susceptible to lysis
S. pneumoniae is a catalase-positive organism which can destroy oxygen radicals
Antibody produced from immunization counteract the cytochrome defect
S. pneumoniae is a catalase-negative organism which can produce hydrogen peroxide
