Chronic oedema

Secretan s syndrome must be differentiated from professional traumatic complaints featuring hard, persistent and spontaneous lymph oedema, which have been described in fishermen, due to various causes and particularly to repeated trauma from sea-urchin spines and the tight cuffs of the wet-suit (Angelini et al. 1990 Angelini and Vena 1991). In these spontaneous, chronic professional cases, lymphography may show alterations of the lymph vessels. Secretan s syndrome must also be differentiated from other types of acute or chronic oedema, such as lymphatic aplasia, recurrent erysipelas, deep thrombophlebitis, angio-oedema, filariasis, venous obstruction, post-surgical disturbances, carcinoma and other tumours of the breast. 

Beri-beri or clinically manifest thiamin deficiency exists in several subforms infantile beri-beri and adult beri-beri. Infantile beri-beri occurs in exclusively breastfed infants of thiamin-deficient mothers. Adults can develop different forms of the disease, depending on their constitution, environmental conditions, the relative contribution of other nutrients to the diet as well as the duration and severity of deficiency. First of all, there is a so called dry or atrophic (paralytic or nervous) form, including peripheral degenerative polyneuropathy, muscle weakness and paralysis. Second, a wet or exudative (cardiac) form exists. In this form, typical symptoms are lung and peripheral oedema as well as ascites. Finally, there is a cerebral form, that can occur as Wernicke encephalopathy or Korsakoff psychosis. Tli is latter form mostly affects chronic alcoholics with severe thiamin deficiency. 

Laboratory evaluation [241] of acute and chronic toxicity of prenylamine indicates that, in high doses, convulsions accompanied by respiratory paralysis (often with pulmonary oedema) led to death. Doses inadequate to produce this result led only to phenomena characteristic of reserpine-like dmgs. Chronic administration failed to produce recognizable changes in any organs or tissues studied. No toxic effects, unattributable to amine depletion, have appeared during several years clinical use. 

T lymphocytes and mast cells are involved in the production of mucus, oedema, smooth muscle hypertrophy and this can lead to mucus production and epithelial damage. If asthma is chronic it can lead to inflammation associated with irreversible bronchoconstriction. 

HT-R antagonist (HIS-R) [for oedema, chronic venous insufficiency haemorrhoids] 5HT-R antagonist - 5HT2-R (HIS-R) [for oedema, chronic venous insufficiency haemorrhoids T GI transit]... 

HIS-R antagonist (5HT-R) [for oedema, chronic venous insufficiency haemorrhoids]... 

Many corticosteroids undergo metabolism via CYP3A4 and are substrates of P-gp. They are used to suppress inflammation in the respiratory tract, reducing mucosal oedema and decreasing bronchial secretions. They are employed both to prevent acute exacerbations of chronic airways disease and to treat acute flare-ups. They may be subject to interactions when administered orally, but interactions with high-dose inhaled formulations are thought to occur due to steroid that is deposited in the oropharynx, swallowed and absorbed via the gastrointestinal tract. 

Oedema disease It has not yet been clarified to what extent the so-called oedema disease, a chronic generalized condition of hydration of the interstitial tissue, may be regarded as a disease in its own right. 

It is not clearly understood why in some cases oedema without ascites and in other cases ascites without oedema as well as ascites together with oedema or even pleural effusion without ascites occur. Ascites develops most frequently during the course of liver disease (= hepatogenic ascites), in particular in chronic liver diseases with portal hypertension (= portal ascites), (s. tab. 16.7) Various mechanical, biochemical and neural disorders overlap in their effects and pathways, depending on the underlying liver disease. Only rarely is ascites found in diseases with presinusoidal localization of portal hypertension (such as portal vein thrombosis) or with minor restrictions in the synthesis of albumin (as in biliary cirrhosis). Formation of ascites occurs in about 50% of all cirrhotic patients within 10 years of... 

Disorders of cerebral functions on the one hand and of the water and electrolyte balance on the other hand are the earliest and most reliable hints of the onset of decompensation in severe liver disease, especially cirrhosis. In clinical terms, they can be easily diagnosed as latent hepatic encephalopathy (by carrying out psychometric tests) and/or latent oedema (by recording the increase in body weight). For this reason, these examination methods are also of fundamental importance in the follow-up of chronic liver disease, (s. fig. 15.3)... 

Ascites and oedema are also found in severe hepatic diseases, pointing to serious disorders in the water and electrolyte metabolism. These complications are signs of decompensation in fiver cirrhosis or chronic liver insufficiency. At the same time, pleural effusion may also be evident. Cirrhosis-related pleural effusion without concomitant ascites has been described as a rarity. (see chapter 16)... 

In the course of acute or chronic liver disease, the biochemical functions of the liver may be compromised indefinitely the outcome is decompensated liver insufficiency. (s. pp 277, 381) (s. tab. 20.4) The stage of decompensation is synonymous with the onset of life-threatening complications. These mainly take the form of hepatic encephalopathy with transition to hepatic coma (see chapter 15), oedema and ascites with imbalance of the electrolytes and the acid-base equilibrium (see chapter 16) through to the hepatorenal syndrome (see chapter... 

Histology provides useful diagnostic evidence. Sinusoidal endothelial damage can be found, including extra-vascular accumulation of erythrocytes in Disse s spaces as well as subendothelial oedema and cellulation. After 2 to 3 days, delicate fibres appear within the central and sublobular veins, occasionally also in the medium-sized hepatic veins, ultimately resulting in occlusion of the lumen. Fibrotic thickening of the vessel walls occurs. Stenosis and thrombosis of the small hepatic veins cause extensive sinusoidal congestion. The liver cells become necrotic or atrophic. Micronodular cirrhosis develops in a chronic course, (s. fig. 29.10)... 

Meyers AM, Feldman C, Sonnekus MI, Ninin DT, MargoUus LP, WhaUey NA. Chronic laxative abusers with pseudo-idiopathic oedema and autonomous pseudo-Bartter s syndrome. A spectrum of metabolic madness, or new lights on an old disease S Afr Med J 1990 78(11) 631-6. 

In contrast to the acute mediator-induced bronchocon-striction and mucosal oedema characteristic of the EAR, there is now considerable evidence that the LAR is associated with inflammatory cell accumulation and activation. This situation is generally considered to be analogous to that seen in chronic airway inflammation, but some caution is needed in extrapolating the results of... 

Possible applications are extensive and include the treatment of pain (e.g. in burns), inflammation, neurogenic inflammation, oedema (including cerebral oedema and angio-oedema), shock (especially septic shock, probably with B, as well as B2 antagonists), rhinitis and asthma, pancreatitis and defective ion transport, such as cholera, Crohn s disease and cystic fibrosis, and chronic inflammatory conditions such as rheumatoid and osteoarthritis. 

Absorption of sodium salts can result in water retention and a rise in blood pressure, and chronic use should be avoided in patients with renal insufficiency, oedema, high blood pressure or congestive heart failure. 

Warm autoimmune haemolytic anaemia may be either idiopathic or secondary to chronic lymphocytic leukaemia, lymphomas, systemic lupus erythematosus, or other autoimmune disorders or infections. Warm autoantibodies are responsible for 48-70% of autoimmune haemolytic anaemia cases and may occur at any age due to the secondary causes, however, the incidence increases starting around 40 years of age. There is an approximate 2 1 female predilection, possibly due to the association with other autoimmune diseases. Warm autoimmune haemolytic anaemia presents as a haemolytic anaemia of varying severity. The symptoms are those of anaemia (i.e. weakness, dizziness, fatigue, pallor, oedema, and dyspnoea on exertion) and haemolysis (i.e. jaundice, dark urine, and splenomegaly). The laboratory evaluation shows a reduced... 

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