Pathology
Inflammatory Responses
Regarding acute inflammation, which of the following statements is CORRECT:
Answer:
Vasodilation occurs resulting in increased blood flow to the injured area (causing redness and heat). Endothelial contraction results in increased fenestrations between endothelial cells and increased permeability of vessels to plasma proteins. Proteins leak out of the plasma into the interstitial space. The combined increase in plasma hydrostatic pressure and decrease in plasma oncotic pressure causes net fluid movement from plasma into tissues (causing oedema). The formation of a fibrin net acts as a scaffold for inflammatory cells, preventing the spread of microorganisms. Neutrophil polymorphs pass between endothelial cell junctions and invade damaged tissue to combat the effects of injury.Acute Inflammation
Pathology / Inflammatory Responses
Last Updated: 8th November 2021
Inflammation is the response of living tissues to cellular injury. The purpose of inflammation is to localise and eliminate the causative agent, limit tissue injury and restore tissue to normality.
Causes
- Physical agents (e.g. trauma, heat, cold, ultraviolet light, radiation)
- Irritant chemicals (e.g. acids, alkali)
- Microbial infections (e.g. pyogenic bacteria)
- Immune-mediated hypersensitivity reactions
- Tissue necrosis (e.g. myocardial infarction)
Classic Signs
- Rubor (redness)
- Calor (heat)
- Dolor (pain)
- Tumor (swelling)
- Functio laesa (loss of function)
These classic signs are produced by a rapid vascular response and cellular events. The main function of these events is to bring elements of the immune system to the site of injury and prevent further tissue damage.
Vascular Response
- Vasodilation
- Vasodilation occurs resulting in increased blood flow to the injured area (causing redness and heat)
- Increased vascular permeability
- Endothelial intracellular proteins contract under the influence of chemical inflammatory mediators such as histamine, serotonin, bradykinin, nitric oxide and leukotriene B4
- Endothelial contraction results in increased fenestrations between endothelial cells and increased permeability of vessels to plasma proteins
- Proteins leak out of the plasma into the interstitial space
- Inflammatory oedema
- The combined increase in plasma hydrostatic pressure and decrease in plasma oncotic pressure causes net fluid movement from plasma into tissues (causing oedema)
- This has several advantages
- Fluid increase in damaged tissue dilutes and modifies the actions of toxins
- Protein levels increase in the tissue - these include protective antibodies and fibrin
- Non-specific antibodies act as opsonins for neutrophil mediated phagocytosis and function to neutralise toxins
- The formation of a fibrin net acts as a scaffold for inflammatory cells, preventing the spread of microorganisms
- Circulation of the exudate into the lymphatic system assists in antigen presentation and helps mount a specific immune response
Cellular Events
Neutrophil polymorphs pass between endothelial cell junctions and invade damaged tissue to combat the effects of injury. The movement of leucocytes out of the vessel lumen is termed extravasation, and is achieved in five phases:
- Margination to the plasmatic zone assisted by the slowing of blood
- 'Rolling' of leucocytes due to the repeated formation and destruction of transient adhesions with the endothelium
- Adhesion of leucocytes to the vascular endothelium, due to the interaction of paired molecules on the leucocyte and endothelial cell surface
- Transmigration of leucocytes passing between the endothelial cell junctions, through the vessel wall into the tissue spaces
- Chemotaxis of neutrophils migrating towards the site of tissue injury, attracted by chemotaxins such as leukotrienes, complement components and bacterial products
Activated neutrophils and monocytes, as well as mast cells, ingest debris and foreign particles at the site of injury. Phagocytosis is assisted by opsonisation with immunoglobulins and complement components. Acute inflammation produces numerous dead bacteria and damaged and dying neutrophils, macrophages and tissue cells situated in a fibrin-rich fluid. Together, this forms the yellow fibrinopurulent exudate known as pus.
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- Biochemistry
- Blood Gases
- Haematology
| Biochemistry | Normal Value |
|---|---|
| Sodium | 135 – 145 mmol/l |
| Potassium | 3.0 – 4.5 mmol/l |
| Urea | 2.5 – 7.5 mmol/l |
| Glucose | 3.5 – 5.0 mmol/l |
| Creatinine | 35 – 135 μmol/l |
| Alanine Aminotransferase (ALT) | 5 – 35 U/l |
| Gamma-glutamyl Transferase (GGT) | < 65 U/l |
| Alkaline Phosphatase (ALP) | 30 – 135 U/l |
| Aspartate Aminotransferase (AST) | < 40 U/l |
| Total Protein | 60 – 80 g/l |
| Albumin | 35 – 50 g/l |
| Globulin | 2.4 – 3.5 g/dl |
| Amylase | < 70 U/l |
| Total Bilirubin | 3 – 17 μmol/l |
| Calcium | 2.1 – 2.5 mmol/l |
| Chloride | 95 – 105 mmol/l |
| Phosphate | 0.8 – 1.4 mmol/l |
| Haematology | Normal Value |
|---|---|
| Haemoglobin | 11.5 – 16.6 g/dl |
| White Blood Cells | 4.0 – 11.0 x 109/l |
| Platelets | 150 – 450 x 109/l |
| MCV | 80 – 96 fl |
| MCHC | 32 – 36 g/dl |
| Neutrophils | 2.0 – 7.5 x 109/l |
| Lymphocytes | 1.5 – 4.0 x 109/l |
| Monocytes | 0.3 – 1.0 x 109/l |
| Eosinophils | 0.1 – 0.5 x 109/l |
| Basophils | < 0.2 x 109/l |
| Reticulocytes | < 2% |
| Haematocrit | 0.35 – 0.49 |
| Red Cell Distribution Width | 11 – 15% |
| Blood Gases | Normal Value |
|---|---|
| pH | 7.35 – 7.45 |
| pO2 | 11 – 14 kPa |
| pCO2 | 4.5 – 6.0 kPa |
| Base Excess | -2 – +2 mmol/l |
| Bicarbonate | 24 – 30 mmol/l |
| Lactate | < 2 mmol/l |
