Acute inflammation Flashcards
What is the biological purpose of acute inflammation?
It is a response to deliver defensive materials, such as blood cells and fluid, to a site of injury in living, vascularised tissue. It protects the body against infection and clears damaged tissue in repair. Lasts only a short time.
What are the major causes of acute inflammation?
Foreign bodies Immune reactions Infections Tissue necrosis Trauma Physical and chemical agents
List and explain the characteristic signs of acute inflammation
Rubor (redness) Color (heat) Tumour (swelling) Dolor (pain) Loss of function
Describe changes to vascular flow during acute inflammation
There is transient vasoconstriction of arterioles followed by mas vasodilatation. This increases blood flow. Blood vessels become more permeable which creates a fluid exudate and slows the circulation causing swelling.
Explain the occurrence of fluid exudate in acute inflammation (Starling’s Law)
Vasodilation of arterioles due to vasoactive mediators (amines) such as histamine, although many others present. This increases flow to capillaries and capillary pressure rises. Venules and endothelia become leaky and plasma escapes. This increases the venule haemocrit, slowing down flow and increasing upstream pressure.
Outline neutrophil infiltration
(1) stasis causes neutrophils to line up at the edge of blood vessels along the endothelium, known as margination. (2) they then roll along the endothelium and stick intermittently, known as rolling (3) they then stick more avidly, known as adhesion (4) they then emigrate through the vessel wall. This is achieved by relaxation of endothelial cell junctions and digestion of the vascular basement membrane.
Outline neutrophil infiltration
(1) stasis causes neutrophils to line up at the edge of blood vessels along the endothelium, known as margination. (2) they then roll along the endothelium and stick intermittently, known as rolling (3) they then stick more avidly, known as adhesion (4) they then emigrate through the vessel wall.
How does acute inflammation aid in injury recovery
(1) fluid exudate delivers plasma proteins to area of injury, dilutes toxins and increases lymphatic drainage. (2) infiltration of cells removes pathogenic organisms, (3) vasodiatation increases delivery and temperature, (4) pain and loss of function increases rest and reduces further chance of traumatic damage.
What is the most common WC in acute inflammation?
Neutrophil (polymorph)
What do neutrophils do?
Phagocytosis; contact, recognise, internalise. This is faciliated by opsonins (C3b and Fc). Phagosomes fuse with lysosomes to produce secondary lysosomes.
What are the important chemical mediators in acute inflammation?
(1) proteases; kinins, complement system, coagulation system (2) prostaglandins; metabolites of arachidonic acid. (3) cytokines; produced by WBC (4) histamine
Explain complications of acute inflammation
Swelling, causing blockage of tubes and ducts. Exudate, can cause compression. Loss of fluid from burns which can lead to dehydration, circulatory problems. Pain and loss of function, especially if prolonged.
Outline the systemic consequences of acute inflammation
(1) Fever, from endogenous pyrogens such as IL-1 and TNFalpha, & prostaglandins. (2) leukocytosis: accelerated release from marrow. Bacterial infections increase neutrophils, viral increase lymphocytes. (3) acute phase response: decreased appetite, raised HR and altered plasma levels of acute phase proteins: CRP, alpha1 antitrypsin, haptoglobin, fibrinogen. (4) spread of microorganisms and toxins which may lead to SHOCK.
Outline neutrophil immigration
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How do neutrophils kill microorganisms? Give examples of O2 dependent and independent.
Phagocytosis. Killing mechanisms are either O2 dependent or independent. Dependent: produces superoxide and hydrogen peroxide. Independent = produces lysozymes and hydrolases, defensins (cationic proteins) and bactericidal permeability increasing proteins (BPIs)
What are the important chemical mediators in acute inflammation?
(1) proteases; kinins, complement system, coagulation system (2) prostaglandins; metabolites of arachidonic acid. (3) cytokines; produced by WBC
Outline neutrophil immigration
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What is the most common WC in acute inflammation?
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How does acute inflammation aid in injury recovery
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What do neutrophils do?
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Outline the systemic consequences of acute inflammation
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Explain, briefly, how neutrophils carry out chemotaxis and phagocytosis
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How do neutrophils kill microorganisms?
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What are the important chemical mediators in acute inflammation?
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Explain complications of acute inflammation
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Outline the systemic consequences of acute inflammation
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List a few examples of acute inflammation, with the organisms which cause them
- Lobar pneumonia
- Acute appendicitis
- Bacterial meningitis
- Ascending cholangitis/ liver abcess
Outline 3 examples of inherited disorders surrounding acute inflammation
- Heriditary angio-oedema
- Alpha-1-antitrypsin deficiency
- Chronic granulomatous disease
Briefly explain Starlings Law and the two factors it describes
increased hydrostatic pressure = increased fluid out of vessel.
increased colloid osmotic pressure of interstitium = increased fluid flow out of vessel
Describe the difference between a transudate and an exudate
Transudates are not high in protein and usually result from an increase in chronic pressure, such as heart failure. The oedema which collects here is usually just plasma. However, exudate is protein rich and occurs in inflammation where vessel walls become more permeable. OEDEMA LEADS TO INCREASED LYMPHATIC DRAINAGE.
How do neutrophils move?
Chemotaxis; movement along concentration gradients of chemoattractants. These can be chemotaxins, receptor-ligand binding, rearrangement of cytoskeleton or production of pseudopod.
What may happen after the development of acute inflammation?
(1) complete resolution, (2) continued acute inflammation with chronic inflammation = abscess (3) chronic inflammation and fibrous repair (4) death.
What may happen after the development of acute inflammation?
(1) complete resolution, (2) continued acute inflammation with chronic inflammation = abscess (3) chronic inflammation and fibrous repair (4) death.
If tissue architecture has been destroyed then complete resolution is not possible.
