AGAPE

  • AddThis Feed Button
  • Calendar

    November 2017
    M T W T F S S
    « Sep    
     12345
    6789101112
    13141516171819
    20212223242526
    27282930  
  • Add to Technorati Favorites
  • Archives

  • Top Posts

  • Blog Stats

    • 27,243 hits
  • Flickr Photos

  • Recent Comments

    best recipes for roa… on dermatomyositis (DM) in an…
    Nida on A new, precise definition of a…
    RadWind on Physical biology
    iskanbasal on Babinski sign
    Jacek on Babinski sign
    drtombibey on Jill Bolte Taylor: My stroke o…
    Emma Jones on PFO Closure has significant im…
  • Top Clicks

    • None
  • Delicious

  • TAGS

  • AddThis Social Bookmark Button
  • visitors

Posts Tagged ‘Medstudent’

Xanthopsia and the distribution of Jaundice in body fluids

Posted by iskanbasal on April 2, 2009

What is it, xanthopsia?

In deep jaundice, the ocular fluids are yellow, and this
is considered to explain the extremely rare symptom of
xanthopsia (seeing yellow).

The wikipedia definition is here:

“Xanthopsia refers to the predominance of yellow in vision due to a yellowing of the optic media of the eye. The most common cause is digoxin toxicity and the development of cataracts which can cause a yellow filtering effect”.

The General Practice notebook definition :

The patient with xanthopsia complains that his vision has a yellow tinge.

Xanthopsia is caused by:

  • severe jaundice
  • digoxin toxicity.

I’m reviewing now the liver diagnostic tests and procedures and have posted about in a previous post. The metabolism of bilirubin and its secretion by the liver is one of the important subjects related to the liver function and testing. I’m reading important notes about bilirubin metabolism and how jaundice is distributed in body fluids. One is the term xanthopsia which in wikipedia is associated with cataracts and digoxin toxicity but not with deep jaundice. Another notes about the distribution of jaundice is that exudate tends to be more icteric than transudates because it contains more protein-bound bilirubin; that urine, sweat, semen and milk contain bile pigment in the deeply jaundiced patient. But most importantly is the fact that bilirubin is readily bound to elastic tissue. Skin, ocular sclera and blood vessels have a high elastic tissue content, and easily become icteric. This also accounts for the disparity between the depth of skin jaundice and
serum bilirubin levels during recovery from hepatitis and cholestasis.

I’m reading on this outstanding textbook of liver diseases, but only few things as it is too much vast:

Diseases of the Liver

and Biliary System by SHEILA SHERLOCK and JAMES DOOLEY

Advertisements

Posted in Lab | Tagged: , , , | Leave a Comment »

Macroenzymes

Posted by iskanbasal on March 31, 2009

Macroenzymes, what are they?

“Macroenzymes are enzymes in plasma that have a higher molecular mass than the corresponding enzyme normally present under (patho) physiological conditions. They may arise through self-polymerization or by association with other plasma components, in particular immunoglobulins”.

This citation from an article:

“A paediatric case of macro aspartate aminotransferase”

Read the article here doi:10.1258/acb.2007.007094 Ann Clin Biochem 2008;45:323-324

Why I’m interested? I encountered this subject during studying for liver function tests after having finished the disorderds of lipid metabolism which I posted about below.

Type-1 macroenzymes result from the formation of antigen-antibody complexes, using GPT, GOT, gama-GT, and AP

Type-2 macroenzymes result from oligomerization using gama-GT, AP, LAP and 5′-NU.

In the absence of clinical findings continuous elevation of measured GPT(and also GOT) is found with the appearance of macroenzymes.




Posted in Lab | Tagged: , , , | Leave a Comment »

Disorders of lipid metabolism

Posted by iskanbasal on March 27, 2009

Or disorders of lipoprotein metabolism. I studied for this subject some chapters from important textbooks of medicine:

1. Chapter 350 from the Harrison’s principles of internal medicine. Clinically is the most comprehensive on the subject, either the description of  diseases of lipid metabolism or the approach to treatment.

2. Chapter 217 from Cecil medicine. Same as the above particularly when telling the physiopathology and the role of nuclear factors such as the PPARalpha, PPAR?, and PPARd in the regulation of lipids in the human body.

3. Chapter 21 “hyperlipidemias” from the Lippincott’s illustrated reviews: pharmacology 4th ed. a good rapid and concise review on the drugs used here.

4. Chapter 5 Tests of lipid metabolism from the Wallach interpretation of diagnostic tests. Excellent tables on this subject from the Adult Treatment Panel III guidelines.

One of the most useful paragraphs on the subject is that where the Harrison’s describes the diagnostic process. Now I should consider the lab results and divide them in categories. The critical first step in managing a lipid disorder is to determine the class or classes of lipoproteins that are increased or decreased in the patient. I might have Lab results showing only increased levels of tryglicerides or only increased levels of LDL-cholesterol and think about the differential diagnosis in each situation. But the most common error in the diagnosis and treatment of lipid disorders occurs in patients with a mixed hyperlipidemia without chylomicronemia. This occurs with increased levels of both cholesterol and tryglyceride which may indicate TypeIII (increased IDL levels) or Type IIb( increased LDL and VLDL) or TypeIV ( increased VLDL levels). Analysis of lab tests is very important to distinguish between the different situations. I also considered the secondary causes of lipid disorders: obesity, Diabetes mellitus, thyroid diseases, renal diseases, liver disorders, alcohol, and endocrine disorders but particularly the role of hyperlipidemia as a major risk for Coronary heart disease. Actually the tests of lipid metabolism ( my initial interest in this subject) has two important objectives:

1. to assess risk of atherosclerosis, especially Coronary heart disease

2. to classify hyperlipidemias.

I reviewed all the other risk factors for coronary heart disease(CHD) and understood the importance in calculating the atherogenic risk in a general practice setting. What I’m doing is to try to build the good and necessary clinical knowledge (CK) that one needs.

Posted in Cardiology, Lab | Tagged: , , , | Leave a Comment »

Prealbumin (PAB)

Posted by iskanbasal on March 17, 2009

First it was established that to assess the nutritional status of a critically ill patient admitted to the ICU or to surgery it was necessary to determine albumin, prealbumin, C -reactive protein and retinol-binding protein. Prealbumin is considered the better choice for this purpose, why?

Albumin has a half-life of 21 days, it is slow to respond to changes while PAB has a half-life of 2 days and respond quickly to any change in the nutritional status of the patients.

Reference values:

Values of 0 to 5, 5 to 10 and 10 to 15 mg/dL indicate severe, moderate and mild protein depletion respectively.

Moreover, I understand that PAB is used to determine in a traumatic patient that the losing liquid from their nose is a cerebrospinal fluid (CSF) by the determination of the concentration of PAB in it.

I’m studying some chapters in lab medicine and diagnostic testing.

Posted in Lab | Tagged: , , | Leave a Comment »

 
%d bloggers like this: