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C-reactive protein (CRP) is a very sensitive acute phase reactant. Serum CRP levels increase following a variety of pro-inflammatory events such as infection, tissue necrosis, trauma, surgery and even malignancy. CRP levels can increase quickly and dramatically (often 100 fold) during inflammation. CRP can activate compliment, bind Fc receptors and can function as an opsonin, enhancing phagocytosis with certain infections. Measurement of CRP is not new, it has been on clinical laboratory testing menus for decades. However, a newer version of the CRP test is now in use to assess cardiovascular risk.High sensitivity-CRP (hs-CRP) assays have been developed that are more sensitive to the more subtle changes that can occur during chronic vascular inflammation. (Recall that atherosclerosis is an inflammatory process.) By measuring hsCRP we can get a glimpse at vascular function. CRP has been shown to be an independent risk factor for atherosclerotic disease and cardiac death. A 2002 prospective study of more than 27,000 patients showed that the CRP concentration is a stronger predictor of cardiovascular events than the LDL-cholesterol level.

Oxidized LDL leads to the release of chemotactic factors from nearby cells; factors which signal leukocytes to migrate to the site. Recall that atherosclerosis is believed to be caused by phagocytic cells such as macrophages, which ingest LDL particles and turn into stationary foam cells. Macrophages have been shown to have increased affinity for oxidized LDL. Thus, oxidation makes LDL more susceptible to phagocytosis and therefore more atherogenic.Since oxidized LDL is more atherogenic than native LDL it makes sense that oxidized LDL may be a cardiovascular risk marker. Indeed, many studies have now correlated increased levels of oxidized LDL with risk of cardiac events.

The major determinant of prognosis in cases of hereditary hemochromatosis (HH) is the degree of organ damage from iron overload at the point of diagnosis. The presence of liver cirrhosis reduces life expectancy. Damage that has occurred to tissues and organs is irreversible, but further damage can be halted with treatment. When there is no evidence of cirrhosis at time of diagnosis, life expectancy may be equal to that of persons without HH. With proper management of HH through treatment, affected individuals have good long-term outcomes. Hepatocellular carcinoma associated with cirrhosis, hepatic failure, and cardiac failure are the most common causes of death in persons with HH. Compared to the normal population, liver cancer is many times more prevalent as a cause of death in persons with HH. Cardiomyopathy, diabetes, and cirrhosis are all more common causes of death among persons with HH than among normal persons. The earlier HH is detected, before the onset of severe organ damage, the lower the risk of mortality.

Example: Hydrogen cyanidePhysical Properties: Highly volatile gas with a bitter almond odor.General Signs and Symptoms: Violent convulsions, stoppage of breathing, cardiac failure.Relative Rate of Action: Incapacitation within minutes and death within 15 minutes.

The degree of electricity-induced injury is dependent on: The amount of electrical energy that is delivered The resistance that is encountered The type of current The current pathway The duration of contact

Four major classes of drugs are frequently monitored by TDM: Antibiotics Anticonvulsants Immunosuppressants Cardiac medicationsThere are other drugs that are monitored by TDM that are not included in any of the above classifications, but the majority of TDM testing is performed for drugs that are included in one of these four categories.