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| − | {{review}}
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| − | {{toplink
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| − | |linkpage =:Category:WikiPath
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| − | |linktext =General Pathology
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| − | |maplink = General Pathology (Content Map)
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| − | |pagetype =Pathology
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| − | |sublink1=Circulatory Disorders - Pathology
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| − | |subtext1=CIRCULATORY DISORDERS
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| − | }}
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| | ==Introduction== | | ==Introduction== |
| | Oedema is NOT a disease; it is the sign of a disease state. | | Oedema is NOT a disease; it is the sign of a disease state. |
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| | ** '''Lungs'''. | | ** '''Lungs'''. |
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| − | ==Local oedema== | + | ==[[Local Oedema|Local oedema]]== |
| | * Local oedema is the local accumulation of excess interstitial fluid. | | * Local oedema is the local accumulation of excess interstitial fluid. |
| | * Caused by disturbance of the balance betwen fluid extravasation and resorption at the level of the capillaries. | | * Caused by disturbance of the balance betwen fluid extravasation and resorption at the level of the capillaries. |
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| | ** Food reaction (delayed). | | ** Food reaction (delayed). |
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| − | ====[[Lungs Circulatory - Pathology#Pulmonary oedema|Pulmonary oedema]]==== | + | |
| | + | [[Category:Circulatory Disorders - Pathology]] |
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| | + | |
| | + | ====[[Pulmonary Oedema|Pulmonary oedema]]==== |
| | * In the normal state, pulmonary alveoli are kept dry by three mechanisms: | | * In the normal state, pulmonary alveoli are kept dry by three mechanisms: |
| | *# Normal "push-pull" mechanism at capillary level. | | *# Normal "push-pull" mechanism at capillary level. |
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| | ** E.g. in Adult Respiratory Distress Syndrome (ARDS). | | ** E.g. in Adult Respiratory Distress Syndrome (ARDS). |
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| − | ==General oedema==
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| − | * General oedema involves subcutaneous and tissue spaces/body cavities.
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| − | * Indicative of severe upset of overall body fluid balance.
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| − | ** Usually one or more vital organ system is abnormal.
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| − | * Requires one or more of the following conditions:
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| − | *# General increase in arteriolar hydrostatic pressure.
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| − | *# Decrease in osmotic pressure of blood.
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| − | *# Increase in tissue fluid osmotic pressure.
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| − | *#* E.g. sodium retention in renal disease.
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| − | *# Increased capillary permeability.
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| − | *#* E.g. due to hypoxic damage.
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| | | | |
| − | ===Types of General Oedema===
| + | [[Category:Circulatory Disorders - Pathology]] |
| − | ====Cardiac oedema====
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| − | * Seen in heart failure.
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| − | ** Shows that cardiac output fails to meet the demands of the tissues throughout the body.
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| − | ** Left-side failure gives pulmonary congestion.
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| − | *** Leads to pulmonary oedema.
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| − | ** Right-side failure gives systemic congestion.
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| − | *** Leads to generalised oedema.
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| − | * Chronic venous congestion develops when cardiac output fails to keep pace with venous return to the heart.
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| − | * Fluid balance is further complicated by secondary renal impairment.
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| − | ** Sodium is retained, triggering the renin-aldosterone loop with further sodium retention.
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| | | | |
| − | ====Renal oedema====
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| − | * Kidney malfunction induces oedema as a consequence of deranged sodium and water handling.
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| − | ** There is often secondary cardiac involvement.
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| − | *** Due to via renin effect on heart and myocardial depressant factor.
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| − | * Causes:
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| − | *# '''Acute glomerulonephritis'''
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| − | *#* Reduction in glomerular filtration rate results in systemic hypertension and retention of excess sodium and water.
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| − | *# '''Nephrotic syndrome'''
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| − | *#* A glomerular filtration defect gives selective heavy loss of plasma proteins (especially albumin)
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| − | *#** Reduction of plasma osmotic potential results in oedema.
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| − | *# '''Acute renal tubular necrosis'''
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| − | *#* Tubules can no longer selectively reabsorb sodium and other electrolytes.
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| − | *#** Water retention with the sodium and urea produces oedema.
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| − | *# '''Fibrosing glomerulonephritis'''
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| − | *#* Causes systemic hypertension and secondary cardiac failure with oedema.
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| − | ====Protein-losing enteropathies====
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| − | * Mucosal damage leads to loss of ability to absorb and retain proteins.
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| − | ** Plasma proteins, especially albumin are lost.
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| − | *** Circulating plasma proteins area therefore reduced, leading to oedema.
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| − | * E.g.
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| − | ** Johne's disease in cattle and sheep.
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| − | ** Ulcerative colitis or regional enteritis in dogs.
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| − | * For more on protein-losing enteropathies, see [[Protein Losing Enteropathy|Protein-Losing Diseases]].
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| − | ====Hepatic oedema==== | + | ==[[General Oedema|General oedema]]== |
| − | * Associated with severe [[Liver - Anatomy & Physiology|liver]] damage.
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| − | ** Liver damage may be:
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| − | *** '''Actue'''
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| − | **** E.g. due to acute fascioliasis or canine viral hepatitis.
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| − | **** Lymphatics and blood vessels of the [[Liver - Anatomy & Physiology|liver]] and [[Peritoneal Cavity - Anatomy & Physiology|peritoneal caivity]] are damaged.
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| − | ***** Results in "overflow" of fluid into the [[Peritoneal Cavity - Anatomy & Physiology|peritoneal cavity]].
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| − | **** Additionally, hepatocyte damage may result in inadequate inactivation of aldosterone.
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| − | ***** Increases sodium retention giving further water accumulation in the abdomen
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| − | *** '''Chronic'''
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| − | **** E.g. metastatic neoplasia or fibrosing hepatopathy (cirrhosis).
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| − | **** Failure to produce plasma proteins leads to osmotic imbalance in the peripheral circulation.
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| − | **** This is seen as subcutaneous oedema.
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| − | ***** E.g. "bottle jaw".
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| | ==Composition of oedema fluid== | | ==Composition of oedema fluid== |
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| | ** '''Ventral subcutaneous oedema''' | | ** '''Ventral subcutaneous oedema''' |
| | * Seen in heart failure in horses and cattle. | | * Seen in heart failure in horses and cattle. |
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| | + | [[Category:Circulatory Disorders - Pathology]] |