Necrosis Information and Courses from MediaLab, Inc.
These are the MediaLab courses that cover Necrosis and links to relevant pages within the course.
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If the atherosclerotic process continues and other risk factors are involved, the lipid core of the plaque grows and pushes the arterial wall out. The myeloperoxidase and metalloproteinases degrade the cellular matrix, thinning the fibrous cap making it capable of tearing. Once there are tears, platelet aggregation and the coagulation cascade begin; thrombi or blood clots become part of the plaque. Further plaque growth and repair leads to occlusion and necrosis of vessels. Varying degrees of pain, cerebral or pulmonary infarction, and/or ischemic heart disease result.
|Terminology Describing Ischemic Heart Disease and Heart Failure|
Descriptions of cardiac biomarkers and their use require knowledge of several terms. These terms and their definitions follow.Acute Coronary Syndrome (ACS) Includes all the ischemic events that can occur in the heart. These events range from angina (where there is no cell death or reversible cell injury) to an AMI with large areas of cell necrosis. A continuum of events that are involved in ACS is illustrated on the page that follows this glossary of terms.Acute Myocardial Infarction (AMI) Commonly referred to as a heart attack. A sudden loss of circulating blood and oxygen that causes necrosis of myocardial tissue. It is most often caused by the narrowing of coronary arteries by atherosclerosis, a thrombus, or dislodged plaque material.Angina Chest pain caused by inadequate supply of oxygen to heart myocardium. It is synonymous with angina pectoris, pectoris meaning chest.Congestive Heart Failure (CHF) Usually, a left ventricular dysfunction resulting from aging, hypertension, atherosclerosis or muscle damage from an AMI or repeated AMIs. In CHF, the heart is not able to effectively pump blood through its chambers and to the body. Fluid accumulates in the lungs and tissues causing edema because less blood leaves through the arteries than what entered the heart from the veins. Electrocardiogram (ECG or EKG) The tracings of the electrical current that passes through the myocardium. The heart contractions are stimulated by this current. In areas of myocyte necrosis, the current does not pass and the tracings display abnormal patterns.Infarction An area of tissue death that occurs due to lack of oxygen. Clogging of an artery will cause dead muscle tissue or infarction.IschemiaAn inadequate blood supply that decreases availability of oxygen. Atherosclerosis is the main cause of myocardial ischemia.
|2007 Guidelines for Cardiac Markers in AMI Diagnosis|
Cardiac troponins are the preferred marker. CK-MB (specified as mass measurement) is an acceptable alternative when cardiac troponins are not available. The 2007 ESC/ACC/AHA guidelines recommend use of cardiac markers to detect myocardial necrosis in the following manner: Elevations of cTnI or cTnT over decision limit on one occasion in the first 24 hours after chest pain. Elevations of CK-MB (specified as mass measurement) over decision limit on two successive samples or one sample that is two times the upper limit of normal during the first hours following chest pain. The CK-MB levels should exhibit a rising or falling pattern to be diagnostic. If the CK-MB levels do not fall, it is likely not an AMI.Healthcare facilities and cardiology staff develop their own criteria for AMI diagnosis and treatment based on these guidelines. Many facilities assay both cardiac troponin and CK-MB biomarkers and may request serial troponin levels to find two elevations similar to guidelines for CK-MB.
|Biomarker Sampling Guidelines|
Blood samples should be collected and assayed in intervals. ESC/ACC guidelines stress the importance of serial sampling. They recommend sampling at presentation of chest pain (baseline), then at 6 - 9 hours, and if these samples are negative and necrosis is still suspected, repeat samples at 12 - 24 hours. Some studies recommend sampling at presentation, 2 - 4 hours, 6 - 8 hours, and at 12 hours.Biomarker measurement should be available 24 hours a day and the results presented within 30 - 60 minutes after sample collection.
CK-isoforms are also markers of myocardial necrosis. Using high voltage electrophoresis, subtypes of CK-MM and CK-MB, CK isoforms, can be isolated. They are released in myocyte necrosis and are not ordinarily in peripheral circulation. CK-MB has 4 isoforms; CK-MB1 and CK-MB2 are released 2-4 hours after chest pain, peak in 6-9 hours and like myoglobin, are early markers of an AMI.CK-isoforms are not widely measured in evaluating chest pain and ACS due to the labor intensive procedure that is required (high voltage electrophoresis). When CK-isoforms are used, most often a ratio of CK-MB2/CK-MB1is reported. A ratio of <1 is negative for myocardial necrosis; a ratio >1.7 is positive for myocardial necrosis.
|Gas gangrene may be seen in infections with all the following clostridia EXCEPT:||View Page|
Newfield RS. Vargas I. Huma Z.: Eikenella corrodens infections. Case report in two adolescent females with IDDM. Diabetes Care. 19:1011-3, 1996 OBJECTIVE: To alert physicians caring for patients with diabetes to the microorganism Eikenella corrodens and to discuss the appropriate preventive and therapeutic measures to take against this potentially morbid opportunistic gram-negative bacilli. CASES: We present two cases of extra-oral E. corrodens infections in adolescent females with IDDM. The first patient had diabetes of four years' duration, which was moderately well controlled. Chronic finger biting resulted in a complex felon that evolved gradually and worsened while the patient received cephalexin orally. Delay in seeking further intervention resulted in necrosis of her distal fingertip and nail bed. The second patient had poorly controlled diabetes for five years. She developed an acute thigh abscess at an insulin injection site that resolved after drainage and intravenous antibiotics. CONCLUSIONS: E. corrodens commonly inhabits the human oral cavity and becomes a pathogen mostly when host defenses are impaired, causing abscesses and infections that are at times fatal. Patients with IDDM are compromised hosts and with daily microtrauma to their skin via glucose monitoring and insulin injections, are prone to develop E. corrodens infections that can be introduced through oral secretions by licking or biting their skin. Educational efforts aimed at preventing exposure of traumatized skin to oral secretions can minimize the risk of E. corrodens infections in compromised hosts. Early intravenous administration of antibiotics, bearing in mind E. corrodens resistance to clindamycin, metronidazole, and other antibiotics, coupled with prompt surgical intervention, is essential in successfully managing E. corrodens infections.
|Identify the urine sediment elements shown by the arrow:||View Page|
|Which one of the following statements about acetominophen metabolism is false?||View Page|
|Which of the following cells when found upon microscopic examination of the urine
would be most indicative of kidney disease:||View Page|
|High Sensitivity-C-Reactive Protein|
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.
|Vaso-occlusive Crisis, Continued|
This painful event of vaso-occlusive crisis often results in tissue necrosis. Organs affected include the bone marrow, brain, lungs, kidneys, liver, and spleen. Disorders that may result include bone and joint pathology, stroke, acute chest syndrome, nephropathies, and infections. Triggering mechanisms for this crisis include infection, fever, acidosis, dehydration, cold temperatures, anxiety, stress, and depression. Adults may experience acute chest syndrome due to pulmonary infarcts caused by sickling in the pulmonary microvasculature, whereas children with sickle cell disease can experience acute chest syndrome due to infections.
|HbS with Other Hemoglobins|
Hemoglobin SC occurs as a double heterozygous condition in less than .5% of African Americans but can be as high as 25% in West Africa. Although HbSC disease may produce a less severe anemia, the chance for retinal hemorrhage and renal and bone necrosis is greater due to increased viscosity. Most persons with HbSC disease have splenomegaly, but significant symptoms usually do not show up until the teenage years.The double heterozygote for HbSD is quite rare and produces an anemia midway in severity between sickle cell disease and sickle cell trait.The rare double heterozygote for HbE produces an anemia similar to Hb S beta-thalassemia.
|Gordon and Sweet's Silver Staining - Diagnostic Applications|
Reticular fibers support body organs like the liver, spleen, and kidney. The Gordon and Sweet's silver staining method is used to demonstrate abnormal reticular fiber patterns that may indicate cirrhosis or necrosis of the liver. This is why reticular stains are often requested on liver biopsies. Abnormal reticular fiber patterns may also indicate the presence of certain tumor types in the liver, spleen, or kidney.
|Adipokines Significant to Metabolic Syndrome|
The adipokines that will be discussed on the following pages include: Tumor necrosis factor-alpha (TNF-a) Interleukin 6 (IL-6) Plasminogen activator inhibitor-1 (PAI-1) Adiponectin Angiotensinogen Leptin Resistin
TNF-alpha (TNF-α) produces different effects as it is secreted; many of these effects are immunological and result in increased inflammation. The original name for TNF, tumor necrosis factor, came from its first discovered activity, tumor regression. TNF-α is synthesized and secreted by adipocytes, macrophages, lymphoid cells, endothelial cells and other body cells.Adipocyte-secreted TNF-α stimulates adipocytes to increase their release of NEFAs and decrease adiponectin synthesis. TNF-α also inhibits insulin activity, leading to insulin resistance. Adipocyte TNF-α secretion is increased in obesity causing an increased insulin resistance in obesity.
|Healthcare (Hospital)-Associated MRSA versus Community-Associated MRSA|
As mentioned in the course introduction, MRSA infections fall into two general types:Healthcare-associated MRSA (HA-MRSA) Infections that occur in people who are, or have recently been, hospitalized. Community-acquired MRSA (CA-MRSA) Infections that are apparently acquired in the community There are a number of factors that distinguish HA-MRSA from CA-MRSA isolates. These factors are summarized in the table below.FactorHA-MRSA CA-MRSAOrigin of strainsNosocomial infectionsFive isolates associated with healthcare settings: USA100, -200, -500, -600, -800USA100 is the predominant isolate while USA 200 is the second most common isolate. USA700 has been isolated in both healthcare and community settings.Evolved from endemic methicillin-susceptible S. aureus (MSSA) strains Two clones, USA300 and USA400, are associated with the majority of CA-MRSA infections in the United States. USA300 has emerged as the most prominent clone and is not found among hospital strains.Genetic lineageIsolates usually carry large SCCmec types I, II or III (34-67 kb)The larger size of SCCmecII and III permits the inclusion of other non-beta-lactam resistance genes so that HA-MRSA strains tend to be multi-drug resistantIsolates carry a smaller SCCmec variant, predominantly type IV (24 kb), less often type V or variant VT. SCCmecIV (except for mecA) does not permit the inclusion of other non-beta lactam resistance genes so that CA-MRSA isolates exhibit resistance to only methicillin and erythromycin and are more often susceptible to other non-beta lactam antibiotics (eg., trimethoprim/sulfamethoxazole (SXT) and clindamycin). Affected populationLargely affects older adults and people with weakened immune systems; those who have undergone surgical procedures are at increased risk. Healthy persons in the general population without established risk factors for MRSA acquisitionClinical syndromesFound at multiple sites, most commonly bloodstream infections, urinary tract infections (UTI) and respiratory tract infectionsPredominantly skin and soft tissue infections (SSTIs), such as abscesses, cellulitis, folliculitis and impetigo and a serious form of pneumoniaGenes for Panton-Valentine leukocidin (PVL) are associated with SCCmecIV; the clinical spectrum of infections caused by CA-MRSA is directly related to the presence of PVL genes, coding for the production of a cytotoxin that causes tissue necrosis and leukocyte destruction.
|Which are true statements regarding hospital-associated methicillin-resistant Staphylococcus aureaus (HA-MRSA) and community-associated MRSA (CA-MRSA)?||View Page|
Toxin Comment Most Likely Means of Dissemination Primary Route of Entry General Signs and Symptoms Laboratory Testing Botulism toxin: Gram stained image of C. botulinum courtesy of CDC Produced by Clostridium botulinum Could be purified and used in a bioterrorist event to contaminate food or aerosolized to cause disease Aerosol Food contamination Inhalation Ingestion Difficulty speaking or swallowing Blurred or double vision Drooping eyelids (ptosis) Dilated pupils Dry mouth, decreased gag reflex Weakening of the reflexes (hyporeflexia) Abnormal sensations such as numbness, tingling, and progressive arm or leg weakness Flaccid paralysis Culture, anaerobic Digoxigen-labeled IgG ELISA to detect A, B, E, and F toxins Mouse Bioassay for all toxin types and to confirm DIG ELISA Ricin toxin: Extracted from Castor beans Inhibits protein synthesis Causes death approximately 72 hours after initial exposure As an aerosol Inhalation Fever Cough Chest tightness Dyspnea Cyanosis Gastroenteritis Necrosis Antibody detection in clinical specimens Clinical testing not performed unless known exposure has occurred
Increased numbers of cuboidal cells are found in renal transplant rejection, acute tubular necrosis (diuretic phase), injuries that interrupt blood flow to the kidney, and acute glomerulonephritis accompanied by tubular damage. Ingestion of various drugs and chemicals may cause significant tubular shedding of these epithelial cells. Cuboidal cells are easily seen in urine in cases of salicylate intoxication.
|Renal Tubular Epithelial Cell|
Another type of epithelial cell is the renal tubular epithelial cell. The proximal and distal convoluted tubules are the sites of origin for one form of these cells. They occur singly and are large (14-60 microns). Papanicolaou stain is useful in distinguishing renal tubular cells from other mononuclear cells in urine. Increased numbers of proximal and distal convoluted renal epithelial cells are seen in cases of acute tubular necrosis and certain drug or heavy metal intoxication.