Myocardial infarction

This is the left ventricular wall which has been sectioned lengthwise to reveal a large recent myocardial infarction. The center of the infarct contains necrotic muscle that appears yellow-tan. Surrounding this is a zone of red hyperemia. Remaining viable myocardium is reddish- brown. This cross section through the heart shows the larger left ventricular chamber and the small right ventricle. Extending from the anterior portion and into the septum is a large recent pale myocardial infarction. The center is tan with surrounding hyperemia. This infarction is "transmural" because it extends through the full thickness of the ventricular wall. The earliest change histologically seen with acute myocardial infarction in the first day is contraction band necrosis. The myocardial fibers are beginning to lose cross striations and the nuclei are not clearly visible in most of the cells seen here. Note the many irregular darker pink wavy contraction bands extending across the fibers. This high power microscopic view of the myocardium demonstrates an infarction of about 1 to 2 days in duration. The myocardial fibers have dark red contraction bands extending across them. The myocardial cell nuclei have almost all disappeared. There is beginning acute inflammation. Clinically, such an acute myocardial infarction is marked by changes in the electrocardiogram and by a rise in the MB fraction of creatine kinase. In this microscopic view of a recent myocardial infarction, there is extensive hemorrhage along with myocardial fiber necrosis with contraction bands and loss of nuclei. This myocardial infarction is about 3 to 4 days old. There is an extensive acute inflammatory cell infiltrate, and many neutrophils are undergoing karyorrhexis. The myocardial fibers are undergoing necrosis so that the outlines of them are not well defined. Few cross striations remain, and cell nuclei are no longer visible. The serum troponin would be elevated. This is an intermediate myocardial infarction of 1 to 2 weeks in age. Note that there are remaining normal myocardial fibers at the top. Below these fibers are many macrophages along with numerous capillaries and little collagenization. At 3 to 4 weeks of age the intermediate myocardial infarction shown involving a papillary muscle at low power above and medium power below have decreasing cellularity along with more prominence of collagen. Note that there are remaining normal red myocardial fibers. Cardiac biomarkers are not positive at this stage and myocardial rupture is unlikely. The degree of cardiac failure depends upon the extent of myocardial loss

The myocardium shown demonstrates pale fibrosis with collagenization following healing of a myocardial infarction. There is minimal cellularity; a few remaining viable red myocardial fibers are present. This stage is reached about 2 months following the initial ischemic event. This collagenous scar is nonfunctional for contraction and will diminish the ejection fraction. Such a scar will not rupture. The heart is opened to reveal the left ventricular free wall on the right and the septum in the center. There has been a remote myocardial infarction that extensively involved the anterior left ventricular free wall and septum. The white appearance of the endocardial surface indicates the extensive scarring. One One complication of a transmural myocardial infarction is rupture of the myocardium. This is most likely to occur in the first week between 3 to 5 days following the initial event, when the myocardium is the softest. The white arrow marks the point of rupture in this anterior-inferior myocardial infarction of the left ventricular free wall and septum. Note the dark red blood clot forming the hemopericardium. The hemopericardium can lead to tamponade. In cross section, the point of rupture of the myocardium is shown with the arrow. In this case, there was a previous myocardial infarction 3 weeks before, and another myocardial infarction occurred, rupturing through the already thin ventricular wall 3 days later. There has been a previous extensive transmural myocardial infarction involving the free wall of the left ventricle. Note that the thickness of the myocardial wall is normal superiorly, but inferiorly is only a thin fibrous wall. The infarction was so extensive that, after healing, the ventricular wall was replaced by a thin band of collagen, forming an aneurysm. Such an aneurysm represents non-contractile tissue that reduces stroke volume and strains the remaining myocardium. The stasis of blood in the aneurysm predisposes to mural thrombosis. . A cross section through the heart reveals a ventricular aneurysm with a very thin wall at the arrow. Note how the aneurysm bulges out. The stasis in this aneurysm allows mural thrombus, which is present here, to form within the aneurysm. The epicardial surface of the heart shows a shaggy fibrinous exudate. This is another example of fibrinous pericarditis. This appearance has often been called a "bread and butter" pericarditis, but you would have to drop your buttered bread on the carpet to really get this effect. The fibrin often results in the the finding on physical examination of a "friction rub" as the strands of fibrin on epicardium and pericardium rub against each other. Microscopically, the pericardial surface here shows strands of pink fibrin extending outward. There is underlying inflammation. Eventually, the fibrin can be organized and cleared, though sometimes adhesions may remain.

BLEEDING IN PATIENTS WITH HEMOPHILIA. CME#2

BLEEDING IN PATIENTS WITH HEMOPHILIA

Hemophilia includes bleeding epitomized by limb- or life-threatening bleeding symptoms, such as hemarthrosis, soft-tissue bleeding, muscle hematomas, retroperitoneal and intracerebral hemorrhage, and postsurgical bleeds. To some degree, the type and the site of bleeding are age dependent (owing to characteristic developmental milestones, such mouthing of objects and mobility) and severity of disease dependent. Neonates with severe hemophilia most commonly present with bleeding after circumcision but may also present with intracranial hemorrhage. In toddlers, bleeding from minor mouth injuries and intracranial and extracranial hemorrhages may occur after minor injuries. As the toddler starts to become more mobile, bleeding into soft tissues, such as buttock hematomas and muscle and joint hemorrhages, may become evident.

Kulkarni and colleagues [1]analyzed infants younger than 2 years of age and found that of 580 children with hemophilia studied, nearly 60% were diagnosed within 3 days of birth, 75% in the first month of life, and 90% by 8 months of age. The diagnosis was established earlier in infants whose mothers were known carriers (median, 1 day) or who had a documented family history (median, 2 days) than in those who presented with bleeding (median, 7 days) or whose maternal carrier status was unknown (median, 152 days). Postcircumcision bleeding was the most common site of first bleed (27.4%), followed by head bleeds in 17% (of which 36.4% had an intracranial hemorrhage).[[1]

Because hemophilia A and B are X-linked conditions, the disease occurs in males and is transmitted by females who may be heterozygous for the gene mutation. Historically, it was assumed that carriers were asymptomatic for bleeding; however, it recently has come to light that many carriers do experience bleeding symptoms. Hemophilia A and B carriers, even those with normal hemostatic levels (>40%), have an increased bleeding tendency, including prolonged skin bleeding, heavy menstrual bleeding, oral bleeding, and excessive bleeding after dental procedures and surgery.[2-4].  Additionally, Sidonio and colleagues[5] showed that carriers of FVIII or FIX deficiency enrolled in the Universal Data Collection project had a reduced mean joint range of motion compared with historic controls from the Normal Joint Study. The data from this study suggest that subclinical bleeding may occur as early as adolescence.

1. Kulkarni R, Soucie JM, Lusher J, et al. Sites of initial bleeding episodes, mode of delivery and age of diagnosis in babies with haemophilia diagnosed before the age of 2 years: a report from The Centers for Disease Control and Prevention's (CDC) Universal Data Collection (UDC) project. Haemophilia. 2009;15:1281-1290. Abstract
2. Olsson A, Hellgren M, Berntorp E, Ljung R, Baghaei F. Clotting factor level is not a good predictor of bleeding in carriers of haemophilia A and B. Blood Coagul Fibrinolysis. 2014;25:471-475. Abstract
3. Paroskie A, Oso O, Almassi B, DeBaun MR, Sidonio RF Jr. Both hemophilia health care providers and hemophilia a carriers report that carriers have excessive bleeding. J Pediatr Hematol Oncol. 2014;36:e224-e230. Abstract
4. Plug I, Willemse J, Rosendaal FR. Bleeding in carriers of hemophilia. Blood. 2006;108:52-56. Abstract
5. Sidonio R F, Mili FD, Li T, et al. Females with FVIII and FIX deficiency have reduced joint range of motion. Am J Hematol. 2014;89:831-836. Abstract

Hemophilia management guidelines CME .#1

INTRODUCTION

Hemophilia A and B are X-linked recessive disorders of coagulation characterized by deficiency of Factor VIII (FVIII) and Factor IX (FIX). Across all ethnic groups, the prevalence of hemophilia A is estimated to be 1 in 5000 males, and that of hemophilia B is 1 in 30,000.[ 1] It is estimated that hemophilia affects approximately 400,000 individuals in the world. Hemophilia A is more common than hemophilia B and represents 80% to 85% of the total hemophilia population. This article reviews the latest understanding of hemophilia and the significant progress that has been made in diagnosis and management during the past several decades.

CLASSIFICATION OF SEVERITY

The severity of disease is classified based on the residual plasma levels of circulating FVIII and FIX. The disease is classified as follows: severe if levels are <1%, moderate for levels of 1% to 5%, and mild for levels between 5% to 40% of normal.^[2] There are some limitations to this classification in that it does not recognize the clinical heterogeneity in bleeding observed in individuals with levels <1%.

It has been observed that 10% to 15% of patients with severe hemophilia as defined by factor levels may have a milder clinical profile.^[3] Additionally, this classification may not distinguish between the bleeding profiles of hemophilia A and B.^[4] Based on inpatient hospital admissions, factor consumption, and rates of joint arthroplasty, some reports suggest that hemophilia B may have a milder bleeding phenotype than hemophilia A,^[5-7] although a more recent study demonstrated that age at first bleed, age at first joint bleed, and age at first factor exposure were similar in patients with hemophilia A vs B.^[8] An additional issue that is unresolved is the classification of individuals with levels of 40% to 50%. Another important point that the current classification does not consider is the potential discrepancy between the 1- and 2-stage assays for FVIII (FVIII levels were lower with the 1-stage assay) in some patients with mild hemophilia A.^[9]

Despite these limitations, the current classification is widely accepted, and there is good correlation between age at diagnosis, age at first bleed/first joint bleed, and age at first treatment and the classification of disease severity based on circulating factor levels in most patients.^[ 10] In general, individuals with mild hemophilia bleed only in response to trauma, such as that experienced during surgery, tooth extractions, or major injuries, whereas patients with moderate hemophilia bleed excessively after relatively minor trauma, and those with severe hemophilia may bleed spontaneously or after trivial trauma.

Long walk to ...freedom. Part One: Getting admitted

Some believe that you become a doctor only after you have got an MBBS degree. In reality, from the time you are admitted into a medical school you become a part of the doctor’s community… the people in white coats!

 ’I solemnly pledge myself to consecrate my life to the service of humanity.

I will use my best judgement to help the sick and do no harm.

I will not give fatal drugs to anyone, even if asked, nor will I suggest any such thing.

I will not divulge the secrets of my patients regarding them as holy……’

There is something very hypocritical about this Hippocratic oath. Hippocrates, the famous Greek physician, must have formulated the oath for his disciples in the field of Medicine in the true interest of humanity and to uphold the sanctity of this noble profession. But now this oath-taking ceremony has been glamorized to befit white coat ceremonies to appease nostalgic minds, or worse still to harass doctors in court.

But then nostalgia and harassment run high in any Medical school. The Professors love to recall the days when they, as medical students, had studied till late in the night and spent the better part of this glorious period of one’s life in the dissection halls, the hospital wards, operation theatres or the library. Having been through this gruesome phase, some of them are sympathetic to the plight of medical students. But then there are some who take it out on this fast emerging strain of stress-resistant medical students who believe they can bunk classes, download video lectures and amazing new mobile apps about the Anatomy of the human body, attend concerts, have a nice time at McDonald’s and study Pharmacology with music in the background.

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Metabolic theory of septic shock

Septic shock is a life threatening condition that can develop subsequent to infection. Mortality can reach as high as 80% with over 150000 deaths yearly in the United States alone. Septic shock causes progressive failure of vital homeostatic mechanisms culminating in immunosuppression, coagulopathy and microvascular dysfunction which can lead to refractory hypotension, organ failure and death. The hypermetabolic response that accompanies a systemic inflammatory reaction places high demands upon stored nutritional resources. A crucial element that can become depleted early during the progression to septic shock is glutathione.
Glutathione is chiefly responsible for supplying reducing equivalents to neutralize hydrogen peroxide, a toxic oxidizing agent that is produced during normal metabolism. Without glutathione, hydrogen peroxide can rise to toxic levels in tissues and blood where it can cause severe oxidative injury to organs and to the microvasculature. Continued exposure can result in microvascular dysfunction, capillary leakage and septic shock .
Read about the Early Goal Directed Therapy EGDT for sepsis management.
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Read about the link between iron and vitamin B12 deficiency and panic attacks. http://adf.ly/1AHkuI

On the off chance that you experience the ill effects of tension or get occasional panic attacks marked by episodes of hyperventilation, you could only be encountering the symptoms of a basic supplement inadequacy that is effortlessly correctable, as per Jonathan Benson of Natural News.

This unquestionably seems to have been the situation with 21 individuals who took an interest in a late study based out of Japan, which recognized an absence of both vitamin B6 and iron among members who experienced panic or hyperventilation episodes.

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Be like the river

Sometimes all  you can do, is not to
dream, expect or obsess.
All you can do, is go with the flow,
And hope for the best.