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Thread: Plasma Cell, alcoholic, liver disease blood picture - blood histology atlas

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    Default Plasma Cell, alcoholic, liver disease blood picture - blood histology atlas

    Practicalities
    Many laboratories will examine a peripheral blood film if an abnormality is detected in the FBC or if the clinical details indicate a requirement. However, if you suspect an underlying blood disorder or parasitic infection, request one directly yourself. The sample should be collected in an EDTA bottle and be as fresh as possible at the time of analysis.

    Abnormalities of erythrocytes
    The red blood cell is a pink biconcave disc-shaped cell, about the size of a small lymphocyte nucleus. Normally, healthy cells are roughly the same size, shape and colour. Morphological abnormalities are rarely specific to one condition; they can occur in a range of problems.

    Abnormalities of leukocytes
    As with erythrocytes, each type of leukocyte has characteristics that can be identified on stained specimens allowing for an easy diagnosis to the well-trained eye. The first thing the haematologist will assess is the absolute number of white cells (see separate article Full Blood Count). If the count is low, subsequent stain and diagnosis may be tricky. If the count is high, an assessment is made of which cell type predominates (ie lymphocytes versus granulocytes) and any abnormal cells - see 'Glossary of terms', below.

    Basic Pathophysiology of Liver Disease
    The basic pathophysiology of all forms of liver disease represents failures of the numerous and complex hepatic metabolic functions. Although there is some variability in basic pathophysiology from one type of liver disease to another, all forms of liver disease can reasonably be called hepatic failure. The signs and symptoms, the natural history, and the rationale of treatment for all forms of liver disease derives from certain relatively simple basic pathophysiologic concepts.

    It should be made clear at the outset that jaundice, an obvious physical sign, sometimes represents problems other than liver disease and is by no means synonymous with it. There are other, far more important and more complex metabolic problems associated with liver disease so that the problem of jaundice will be dealt with only briefly in this minicourse. The liver plays several complex roles in amino acid metabolism, protein synthesis, carbohydrate metabolism and lipid metabolism. It is also the site of manufacture of a number of blood coagulation proteins.

    The basic derangements of hepatic failure will be discussed first. These will then be applied to the most common forms of liver disease, acute hepatitis and cirrhosis.
    Plasma Cell, alcoholic, liver disease attachment.php?s=fd2e1cc366981f2c9ca9362b723d6fa4&attachmentid=1432&d=1439594382

    The liver is responsible for detoxifying, by chemical modification, many substances that enter it. This includes substances drained from the gut, many kinds of drugs, and circulating hormones. Some substances are converted to water soluble salts or esters and are excreted in the bile. Others are chemically modified and released into the general circulation for renal excretion. Sometimes, toxic substances are modified, released into the bile, excreted into the gut, reabsorbed from the gut in their modified form, and later find their way to the kidneys for renal excretion.

    The two classic examples of the liver's role in detoxification are the effect of phenobarbital on the liver and estrogen degradation by the liver. It has been observed that the chronic ingestion of phenobarbital results in an increase in the amount of hepatocytic endoplasmic reticulum, presumably indicating a response to the presence of a toxic substance. Estrogen degradation, or lack of it, is best demonstrated in the alcoholic male who, unable to modify and excrete his circulating estrogens, develops gynecomastia,

    telangiectasis (e.g. spider angiomata) and other signs of feminization.

    Alcohol is not the only drug that is toxic to the liver. Many kinds of drugs in wide use are hepatotoxic and, since these hepatotoxic drugs may have to be degraded for excretion by an already diseased liver, their use in advanced or in severe acute liver disease must be approached with caution. The list of drugs that require caution for this reason is enormous.

    The basic problem in acute hepatitis is a widespread inflammatory reaction throughout the liver. This results in edema and congestion, and these compromise hepatic function. Kupffer cell functions are impaired. Hepatocyte functions are impaired. Formation and excretion of bile is impaired. In every case, all of the basic pathophysiologic mechanisms already discussed become operative. In other words, every case of acute hepatitis represents acute hepatic failure with all of its attendant interruptions of normal physiologic functions. The pathologic changes (tissue changes) that occur within the liver itself include hepatocyte necrosis, hyperplasia of the Rupffer cells, and some microscopic anatomic changes. As the liver becomes edematous and engorged, bile canaliculi become obstructed, and bile stasis develops. This undoubtedly contributes further to degeneration of liver tissue.

    Most of the basic pathophysiologic problems in infectious hepatitis are transitory. They disappear after the infection has cleared and after hepatic anatomy returns to normal. In a more severe infection with extreme, widespread acute inflammation and edema, there may be some residual impairment of hepatic function.

    References:
    Liver Failure. Signs and Symptoms | Patient
    Liver Disease











    Last edited by Medical Photos; 08-14-2015 at 11:19 PM.

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