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21 Cards in this Set
- Front
- Back
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What are the systemic effects of inflammation
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Fever
shock leukocytosis leukopenia Acute phase reponse |
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Fever
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Bacterial products stimulate production of IL-1, IL-6, and TNF-alpha cytokines with pyrogenic properties
IL-1 stimulates PGE2 synthesis in hypothalamus and increases body temperature Can be inhibited by aspirin IL-6 and TNF-alpha directly stimulates hypothalamus |
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Shock
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Massive sepsis stimulates TNF-alpha release
Can result in generalized vasodilation and increased endothelial cell permeability resulting in loss of intravascular volume Leads to hypotension and shock |
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Leukocytosis
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Increase in circulating numbers of leukocytes
Increase in IL-1 and TNF-α promotes leukocyte release from the marrow as well as release of specific CSFs (colony stimulating factors). |
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Neutrophilia
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Type of leukocytosis
Increase in PMN number usually due to bacterial infection. “Shift to the left” or increase in “bands” denotes an increase in circulating immature PMNs. |
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What does increase “Shift to the left” or increase in “bands” denote?
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denotes an increase in circulating immature PMNs.
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Lymphocytosis
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Type of leukocytosis
Iincrease in lymphocytes usually associated with viral infections |
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Eosinophilia
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Type of leukocytosis
Increase in eosinophils due to allergic reactions or parasitic infections |
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Leukopenia
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decrease in total circulating leukocyte count associated with chronic inflammation in malnourished individuals or in malignancy
Not understood |
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Acute phase response
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Primitive, systemic host response to infection, inflammation, trauma or malignancy
Includes: Altered lipid metabolism Hypoferemia Glyconeogenesis Induction of acute phase proteins |
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Acute phase proteins
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Component of acute phase response
Synthesized in liver in response to local release of pro-inflammatory cytokines like IL-1, IL-6, and TNF-alpha by monocytes/macrophages or PMNs Includes C-reactive protein, serum amyloid A, fibrinogen, and haptoglobin whose serum concentrations increase by 25% & albumin and transferrin whose serum concentration decrease by 25% |
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What acute phase proteins increase with inflammation
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C-reactive protein, serum amyloid A, fibrinogen and haptoglobin
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What acute phase proteins decrease with inflammation
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Albumin and transferrin
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C-Reactive Protein
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CRP
Member of pentraxin gene family Named due to high affinity binding to pneumococcal C-polysaccharide Binds to phosphotidyl choline and phosphotidyl ethanolamine of cell membrane, chromatin, laminin, fibronectin Activates classical complement pathway Binds to CRP receptors on macrophages, moncytes and PMN to engulf particle CRP was attached too (opsonization) Associated with atherosclerotic complications Routinely monitored as systemic marker for inflammation CRP <10mg/L are normal CRP >100g/L are associated with acute bacterial infection Aspirin, NSAIDS and statins decrease CRP |
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Atherosclerosis
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Injury at local area in vasculature
Inflammatory response begins Becomes trap for cholesterol Monocytes phagocytose lipids and are called Foam Cells due to excessive lipid vacuoles Synthesis of fibrous cap to wall off lipids from circulatory system If MMP-8 is activated by inflammatory cells, fibrous cap is eroded releasing lipids leading to massive clotting and myocardial infarction |
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What is the first histopathological evidence of atherosclerotic lesion
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Foam cells
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What chronic diseases are associated with severe periodontitis?
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Low-birth weight babies
Diabetes mellitus Atherosclerotic complications including myocardial infarction and stroke Rheumatoid arthritis, chronic kidney disease and Alzheimer's disease |
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What are possible mechanisms to explain association of periodontal infections with systemic disease
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1. Seeding of subgingival bacterial species into the circulation to distant sites of inflammation
2. Production of activated inflammatory cells that migrate through sites of chronic inflammation 3. Association is due to presence of confounding factors that are common to both diseases like smoking 4. Generation of an acute phase response by moderate/severe periodontitis |
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"High normal" CRP levels have been associated
with increased risk for myocardial infarction. For example, apparently healthy subjects in the Physician's Health Study that were in the highest CRP quartile at study entry had a greater than 4-fold increased risk myocardial infarction after 4 years compared to the lowest CRP quartile (Ridker et al NEJM, 1997; 336: 973). This risk was reduced by half by the daily administration of: |
325mg of aspirin/day
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What conclusion did PM Rikers 2005 discover after decreasing CRP levels through statins
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Statins lowers the risk of subsequent myocardial infarction
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What conclusion did m Tonetti 2004 discover after completing periodontal therapy
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It only decreased CRP and IL-6 levels
No effect on myocardial infarctions |
