SYSTEMIC EFFECTS OF ACUTE INFLAMMATION

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Presentation transcript:

SYSTEMIC EFFECTS OF ACUTE INFLAMMATION

Systemic manifestation of inflammation 1. Increase of body temperature (fever) 2. Acute phase reaction

Increase of body temperature (fever) Pyrexia (Fever) Polymorphs and macrophages produce compounds known as endogenous pyrogens which act on the hypothalamus to set the thermoregulatory mechanisms at a higher temperature. ‘Endogenous pyrogens’ produced: IL1 and TNFa IL1 - prostaglandins in hypothalamus hence aspirin etc. reduce fever

Increase of body temperature (fever) Release of endogenous pyrogen is stimulated by phagocytosis, endotoxins and immune complexes. Constitutional symptoms Constitutional symptoms include; malaise, anorexia and nausea. Weight loss is common when there is extensive chronic inflammation. For this reason, tuberculosis used to be called 'consumption

SYSTEMIC EFFECTS OF ACUTE INFLAMMATION Haematological changes: Increased erythrocyte sedimentation rate. An increased erythrocyte sedimentation rate is a non-specific finding in many types of inflammation. Leukocytosis IL1 and TNFa produce an accelerated release from marrow Macrophages, T lymphocytes produce colony-stimulating factors Bacterial infections - neutrophils, viral - lymphocytes Clinically useful

Haematological changes Neutrophilia occurs in pyogenic infections and tissue destruction; Eosinophilia in allergic disorders and parasitic infection; Lymphocytosis in; chronic infection (e .g. tuberculosis), many viral infections and in whooping cough; and monocytosis occurs in infectious mononucleosis and certain bacterial infections (e.g. tuberculosis, typhoid)

Haematological changes Anaemia. This may result from blood-loss in the inflammatory exudate (e.g. in ulcerative colitis), haemolysis (due to bacterial toxins), and 'the anaemia of chronic disorders' due to toxic depression of the bone marrow.

SYSTEMIC EFFECTS OF ACUTE INFLAMMATION Amyloidosis Longstanding chronic inflammation (for example, in rheumatoid arthritis, tuberculosis and bronchiectasis), by elevating serum amyloid A protein (SAA), may cause amyloid to be deposited in various tissues resulting in secondary (reactive) amyloidosis

SYSTEMIC EFFECTS OF ACUTE INFLAMMATION Acute phase response Decreased appetite, altered sleep patterns and changes in plasma concentrations of: Acute phase proteins: C-reactive protein (CRP) (Clinically useful) 1 antitrypsin Haptoglobin Fibrinogen Serum amyloid A protein

The acute phase proteins Induction of the acute phase reaction means changes in the synthesis of many proteins which can be measured in plasma. Regulation of protein synthesis takes place at the level of both transcription (DNA, RNA) and translation to protein. The cells have intricate systems for up- and down-regulation of protein synthesis, initiated by a complex system of signals induced in the acute phase reaction.

The acute phase proteins Most of the proteins with increased serum concentrations have functions which are easily related to limiting the negative effects of the acute phase stimulus or to the repair of inflammatory induced damage. Examples are enzyme inhibitors limiting the negative effect of enzymes released from neutrophils, scavengers of free oxygen radicals,

The acute phase proteins increase in some transport proteins and increased synthesis and activity of the cascade proteins such as coagulation and complement factors. The synthesis may be upregulated even if plasma levels are normal, due to increased consumption of acute phase proteins.

Induction and synthesis of CRP in hepatocytes.

CRP functions Most functions of CRP are easily understood in the context of the body's defences against infective agents. The bacteria are opsonised by CRP and increased phagocytosis is induced. CRP activates complement with the split product being chemotactic, increasing the number of phagocytes at the site of infection. Enzyme inhibitors protect surrounding tissue from the damage of enzymes released from the phagocytes.

General and local clinical symptoms of the acute phase reaction General symptoms Local symptoms fever calor increased heart rate rubor hyperventilation dolor tiredness tumor loss of appetite functio laesa

CRP functions CRP binds to chromatin from dead cells and to cell debris which are cleared from the circulation by phagocytosis, either directly or by binding to Fc-, C3b- or CRP-specific receptors. Platelet aggregation is inhibited, decreasing the possibility of thrombosis. CRP binds to low density lipoprotein (LDL) and may clear LDL from the site of atherosclerotic plaques by binding to cell surface receptors on phagocytic cells.

Typical changes of CRP,fibrinogen, ESR and albumin during an acute phase reaction

Systemic effects of acute inflammation '. Reactive hyperplasia of the reticulo-endothelial system Local or systemic Iymph node enlargement commonly accompanies inflammation, while splenomegaly is found in certain specific infections (e.g. malaria, infectious mononucleosis).