Codeine constipation
Codeine is a drug which is well known to cause constipation. Codeine is also known as 3-methoxymorphine. It does not have euphoric effects and so it is freely available over the counter. But it only has 20% of the analgesic potency of morphine. (With in the body codeine is converted morphine by an enzymatic reaction) So it is used to treat mild types of pain such as headache, backache and toothache etc.
Codeine constipation is due to its effect on the gastrointestinal tract. It increases the tone and reduces the motility in many parts of the gastro intestinal tract. Since this reduces the gastric emptying and reduces the rate of movement of food in the gastro intestinal tract this produces small amount of hard stools due excessive water absorption. Sometimes codeine constipation can be very severe and troublesome to the patient. Constipation is thought to be mediated by the effect of codeine on gastro intestinal tract smooth muscle cells. Some suggests that it is mediated by the effect on intramural nerve plexuses. Other hypothesis suggests that constipation is partly mediated by its central effect since intra ventricular injection of codeine inhibits the propulsive movements of the gastro-intestinal tract.
Monday, March 30, 2009
Codeine constipation
Elevated CPK Enzyme
Elevated CPK enzyme level is of great diagnostic value. CPK enzyme is a non functional plasma enzyme and in most of the times elevated levels indicates as underlying organic skeletal muscle disorder or a myocardial infarction. CPK enzyme has 3-isoforms.
CK-BB (Mainly found in the brain tissue)
CK-MB (Mainly found in the myocardial tissue)
CK-MM (Mainly found in the skeletal muscle issue)
Myocardial tissue is the only tissue that contains more than 5% of the total CK-MB activity. So elevated plasma levels of CK-MB isoform of CPK-enzyme suggest a myocardial infarction. But however this should be used along with another cardiac marker like Troponin I ot Troponin T since cpk enzymes coming from the other sources such as skeletal muscle can interfere with the interpretation of the results.
In the case of a myocardial infarction CPK enzyme levels start to rise to rise 4 to 8 hours after the onset of the chest pain and plasma CPK enzyme level reaches the peak in 24 hours.
Serum CPK enzyme is greatly elevated in many muscle disorders including Duchenne dystrophy and polymyositis.But the CPK enzyme level is not elevated in myasthenia gravis and LEMS. In muscle trauma plasma level of myoglobin is also elevated.
