 Hello everyone. Welcome back to another session in Dentistry and more. Today we have a topic from oral pathology. It also comes in general medicine that is a granulocytosis. A granulocytosis before moving on. Let's see what is granulocytes and a granulocytes. So we know blood cells. We can classify blood cells as granulocytes and a granulocytes. Granulocytes are those cells which has granules in the cytoplasm and a granulocytes those without granules in the cytoplasm. So granulocytes are neutrophils, then esophils and basophils. Whereas a granulocytes are lymphocytes and monocytes. So we are studying about a condition where the granulocytes are not properly present. Since we have these granulocytes here, we might get confused about a granulocytosis but we are actually studying about granulocytes. The conditions where the granulocytes are less in number. Okay, that is what a granulocytosis is all about. So it is also known as neutropenia. Penia means less than normal. Then a granulosis, then granulopenia, granulocytopenia. So the most common condition is neutropenia. That is why it is commonly known as neutropenia. Mostly it is a reaction to the Greeks. Regarding the gender prediction, a granulocytosis occurs slightly more frequent in women than in men, possibly because of their increased rate of medication usage. Whether this high frequency is related to the increased incidence of autoimmune disease in women is actually unknown. That is also a possibility. Now moving to the age, it is actually occurs in all age groups. The congenital forms are most common in childhood and this is congenital are mostly seen in childhood. Whereas the acquired is most common in the elderly population. So that was about the age. Now the classification. So it can be congenital meaning a person is born with the condition and person can acquire it from certain drugs or medical procedures. So basically we have two types of classification. Congenital, congenital and acquired. Okay. So what are the causes of neutropenia or a granulocytosis? It is most commonly it is drug induced. Then autoimmune diseases then could be due to infections, viral, protozoa and miscellaneous problems. In autoimmune diseases we have the systemic lupus, erythematosus, SLA, then paltes syndrome, the enteric fever, septicemia, tropaculosis, HIV, the viral problems, again HIV, hepatitis B, Epstein-Bau virus infection, protozoa, malaria, carnazzar, miscellaneous it includes a plastic anemia, then hypersplenism, aglopelastic anemia, chronic autoimmune, neutropenia, cyclic neutropenia. All this comes under autoimmune. Whereas the drug induced antibacterial chloramphenicol, carotrimoxazole, penicillin, oxacycline, cyprofloxacin, gentamicin, anti-inflammatory ibuprofen, phenyl butyzoin, anti-thyroid, tyrosil and carbazol, anti-convulsants, phenytoin, valproic acid. So all can be reasons for a granulocytosis. Now the pathogenesis. Okay, pathogenesis, it could be categorized into four. One is inadequate or inadequate or ineffective formation of granulocytosis, or accelerated destruction of neutrophils, or decreased production, then decreased survival. Okay, let's see one by one. With regard to inadequate or ineffective formation of granulocytes, this can be due to bone marrow failure such as that occurs in plastic anemia, several leukemia and chemotherapeutic agents. So it is seen in aplastic anemia, various leukemia, or chemotherapeutic agents, one accelerated destruction of neutrophils. Okay, so immune-mediated reaction to neutrophils which can be caused by drugs. Okay, so an enlarged spleen can lead to spleenic sequestration and accelerated removal of neutrophils. If there is enlarged spleen, we can expect an accelerated destruction of neutrophil and utilization of neutrophils can also occur in infection. Okay, in all these cases we can see an accelerated destruction of neutrophil. Whereas decreased production is associated with a few syndromes such as cost man's syndrome, then Swatchman diamond syndrome in all these syndromes, what happens is there is decreased production. And also it could be due to leukemia, lymphoma, or plastic anemia, or chemicals, drug-induced one infections. In these cases also there will be decreased production. Decreased survival associated with again few syndromes such as Felte syndrome, Felte syndrome, and autoimmune neutropenia, SLE and also some drugs. So what are the clinical features? Clinical features it depends upon the degree of neutropenia and most commonly it is asymptomatic, chance of high-grade fever, rigorous or throat oral ulcers, abscesses, poor wound healing. So all these can be symptoms and lab diagnosis mostly it will be diagnosed by the blood smear that is a blood examination and also bone marrow examination. So in blood examination there will be acute neutropenia. And regarding the management, the first thing is colony-stimulating factors. So use of growth factors such as glandulocyte, colony-stimulating factors or glandulocyte, macrophage, colony-stimulating factor and erythropoietin can be effective in increasing neutrophil production. And use of antibiotics, combination of broad spectrum antibiotics are usually administered in case of viral and bacterial infection that is about antibiotics then corticosteroids may be used if the cause is an immunological disorder. Okay, so that was about a granular cytosis. So we learned about its introduction and when it is called a tropenia and why it is called a neutropenia and there are various names before that we studied about granular sites, granular sites and when and how it is called neutropenia then regarding the sex and age the classification its causes and regarding the pathogenesis for mechanisms its clinical features lab diagnosis and finally management. That's all for today. 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