Acute Inflammation Flashcards
Acute inflammatory response cardinal signs
Redness- increased blood flow, instigated by arteriolar dilation
Swelling- increased permeability of blood vessels. Vessels invariably affected are venues and sometimes capillaries but arterioles can also leak of damage is severe enough.
Heat- increased blood flow
Pain- damage to nerve pain fibres and release of chemical mediators that induce pain. Include bradykinin (from plasma), serotonin and certain prostaglandins (both from cells). Also from increased tissue tension.
Loss of function- due to death of cells and or swelling which restricts movement.
Leukocytes involved
Polymorphs
- neutrophils- first leukocyte at the scene and only last a few days. Neutral staining granules.
- eosinophils
- basophils
Macrophages
Second type of leukocyte to infiltrate tissue in AIR. Can survive in tissue for extended periods of time. Main purpose is phagocytosis
Other important cells in inflammation
Mast cells- derived from bone marrow, found in connective tissue. Synthesise and secrete many mediators that are involved. Histamine most commonly, causing arteriolar dilation and increases permeability of venules and capillaries in acute inflammation. Also produces heparin, serotonin and prostaglandins.
Mast cell degranulation occurs in tissue trauma as well as in allergic reactions.
Platelets- contain and release many substances, particularly serotonin which can induce vasoconstriction and pain.
Injured and dying native cells-
Epithelial
Fibroblasts- most abundant connective tissue, form collagen, elastic and ground substance
Endothelial cells- line blood vessels
Exudate
Fluid that accumulates in the extra cellular fluid. Process of forming this is called exudation. Comprised of plasma, various levels of plasma proteins and leukocytes.
Degrees of tissue damage will cause 3 manifestations of vascular permeability resulting in distinct types of exudates.
Immediate transient permeability
Increase immediately but short lived.
Mild injuries, results in small gaps between endothelial cells in venules. Gaps due to endothelial cell contraction and largely elicited by histamine from mast cells. This allows plasma and small proteins bw gaps into interstitial fluid.
Serous exudate ensues. Clear with little plasma protein and few leukocytes in it.
Delayed prolonged permeability
Vascular permeability delayed and then protracted. Eg. Sunburn.
Gaps between endothelial cells in venules and capillaries can be large and leak large amounts of plasma and plasma proteins.
Large plasma proteins such as fibrinogen enter the extra cellular tissue and get converted to fibrin.
Fibrinous exudate ensued, indicated higher degree of damage than serous.
Fibrin is normally lysed by the enzyme plasmin, which is generated when we form fibrin.
Immediate prolonged permeability
Vascular permeability is increased immediately and remains for a long time.
Most severe injury, results in damage to all small blood vessels (venules, capillaries, and arterioles) and causes extensive leakage that can result in a fibrinous exudate or if in very severe trauma a combine fibrinous/ haemorrhagic exudate
Suppurative/ purulent exudate
Mainly instigated by bacteria.
Large numbers of polymorphism infiltrate tissue to produce a white/ yellow exudate, pus.
Gaps between endothelial cells in venules and capillaries are quite large so large proteins such as fibrinogen will also escape into interstitial tissue to be converted to fibrin. Therefore, may lead to formation of scar.
Chemotaxis
The movement of cells along a chemical gradient.
Mediators from cells: histamine
Vasodilation
Increased permeability of venules
Mediators from cells: serotonin
From platelets, cause vasoconstriction
Beneficial effects of acute inflammation
Rid body of microbial infection
Remove dead cells in prep for healing
Create memory of foreign invaders
Harmful effects of acute inflammation
May increase blood loss
Pain
Swelling may block hollow tubed organs
Swelling may reduce function of joints
Inflammation
Vascular and cellular response to injury. -itis Acute- lasts a few weeks Sub acute - 3-4 weeks Chronic- months to years