Archive for the tag: Pathophysiology

Diabetic Ketoacidosis (DKA) Pathophysiology, Animation

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Diabetic ketoacidosis (one of the hyperglycemic crises), DKA, pathophysiology, causes, clinical presentation (signs and symptoms) and treatment. This video is available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/narrated-videos-by-topics/diabetes/-/medias/bda71a7a-4598-4b1d-b298-ed06b3c54238-diabetic-ketoacidosis-dka-narrated-animation
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Diabetic ketoacidosis, DKA, is an ACUTE and potentially life-threatening complication of diabetes mellitus. DKA is commonly associated with type 1 but type 2 diabetics are also susceptible. DKA is caused by a critically LOW INSULIN level and is usually triggered when diabetic patients undergo further STRESS, such as infections, inadequate insulin administration, or cardiovascular diseases. It may also occur as the FIRST presentation of diabetes in people who did NOT know they had diabetes and therefore did NOT have insulin treatment.
Glucose is the MAJOR energy source of the body. It comes from digestion of carbohydrates and is carried by the bloodstream to various organs. Insulin is a hormone produced by beta-cells of the pancreas and is responsible for DRIVING glucose INTO cells. When insulin is DEFICIENT, glucose can NOT enter the cells; it stays in the blood, causing HIGH blood sugar levels while the cells are STARVED. In response to this metabolic starvation, the body INcreases the levels of counter-regulatory hormones. These hormones have 2 major effects that are responsible for clinical presentation of DKA:
– First, they produce MORE glucose in an attempt to supply energy to the cells. This is done by breaking down glycogen into glucose, and synthesizing glucose from NON-carbohydrate substrates such as proteins and lipids. However, as the cells CANNOT use glucose, this response ONLY results in MORE sugar in the blood. As blood sugar level EXCEEDS the ability of the kidneys to reabsorb, it overflows into urine, taking water and electrolytes along with it in a process known as OSMOTIC DIURESIS. This results in large volumes of urine, dehydration and excessive thirst.
– Second, they activate lipolysis and fatty acid metabolism for ALTERNATIVE fuel. In the liver, metabolism of fatty acids as an alternative energy source produces KETONE bodies. One of these is acetone, a volatile substance that gives DKA patient’s breath a characteristic SWEET smell. Ketone bodies, unlike fatty acids, can cross the blood-brain barrier and therefore can serve as fuel for the brain during glucose starvation. They are, however, ACIDIC, and when produced in LARGE amounts, overwhelm the buffering capacity of blood plasma, resulting in metabolic ACIDOSIS. As the body tries to reduce blood acidity by EXHALING MORE carbon dioxide, a deep and labored breathing, known as Kussmaul breathing may result. Another compensation mechanism for high acidity MOVES hydrogen ions INTO cells in exchange for potassium. This leads to INcreased potassium levels in the blood; but as potassium is constantly excreted in urine during osmotic diuresis, the overall potassium level in the body is eventually depleted. A blood test MAY indicate too much potassium, or hyperkalemia, but once INSULIN treatment starts, potassium moves BACK into cells and hypokalemia may result instead. For this reason, blood potassium level is monitored throughout treatment and potassium replacement is usually required together with intravenous fluid and insulin as primary treatment for DKA.
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(USMLE topics) What is Gestational Diabetes? Pathology, Risk factors, Complications and Treatments. This video is available for instant download licensing here : https://www.alilamedicalmedia.com/-/galleries/narrated-videos-by-topics/common-ob-gyn-problems/-/medias/257bea34-3735-471b-86d3-d514baa666e8-gestational-diabetes-narrated-animation
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Gestational diabetes is a transient form of diabetes mellitus some women may acquire during pregnancy. Diabetes refers to high levels of blood glucose, commonly known as blood sugar. Glucose is the major energy source of the body. It comes from digestion of carbohydrates and is carried by the bloodstream to the body’s cells. But glucose cannot enter the cells on its own; to do so, it requires assistance from a hormone produced by the pancreas called insulin. Insulin induces the cells to take up glucose, thereby removing it from the blood. Diabetes happens when insulin is either deficient or not used effectively. Without insulin, glucose cannot enter the cells; it stays in the blood, causing high blood sugar levels.
During pregnancy, a temporary organ develops to connect the mother and the fetus, called the placenta. The placenta supplies the fetus with nutrients and oxygen, as well as produces a number of hormones that work to maintain pregnancy. Some of these hormones impair the action of insulin, making it less effective. This insulin-counteracting effect usually begins at about 20 to 24 weeks of pregnancy. The effect intensifies as the placenta grows larger, and becomes most prominent in the last couple of months. Usually, the pancreas is able to adjust by producing more insulin, but in some cases, the amount of placental hormones may become too overwhelming for the pancreas to compensate, and gestational diabetes results.
Any woman can develop gestational diabetes, but those who are overweight or have family or personal history of diabetes or prediabetes are at higher risks. Other risk factors include age, and having previously given birth to large babies.
While gestational diabetes usually resolves on its own after delivery, complications may arise if the condition is severe and/or poorly managed.
Because of the constant high glucose levels in the mother’s blood, the fetus may receive too much nutrients and grow too large, complicating the birth process, and a C-section may be needed for delivery.
High levels of glucose also stimulate the baby’s pancreas to produce more insulin than usual. Shortly after delivery, as the baby continues to have high insulin levels but no longer receives sugar from the mother, the baby’s blood sugar levels can drop suddenly and become exceedingly low, causing seizures. The newborn’s blood sugar level must therefore be monitored and corrected with prompt feeding, or if necessary, with intravenous glucose.
High blood sugar may also increase the mother’s blood pressure and risks of preterm birth. Future diabetes in both mother and child is also more likely to occur.
Gestational diabetes can be successfully managed, or even prevented, with healthy diets, physical exercise, and by keeping a healthy weight before and during pregnancy. In some cases, however, medication or insulin injection may be needed.
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Gestational Diabetes – Overview, signs and symptoms, pathophysiology, diagnosis, treatment

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Pathophysiology of type 2 Diabetes Mellitus

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Pathophysiology of type 2 Diabetes Mellitus

This video is about pathogenesis or pathophysiology of diabetes mellitus. Pathophysiology of diabetes mellitus is explained with the help of graph in relation to fasting blood sugar and insulin resistance. pathogenesis of diabetes mellitus in reference to insulin resistance is explained.

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Criteria for diagnosis of diabetes mellitus

Polyol pathway

Diabetes mellitus diagnostic tests

Glycemic index

Pathophysiology of diabetes ketoacidosis

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Mehr über Diabetes Mellitus nachlesen ⏩ https://bit.ly/DiabetesMellitus_Blog
Der Begriff Diabetes mellitus bezeichnet eine Gruppe von Stoffwechselerkrankungen, bei denen der Glukosegehalt im Blut erhöht ist. Die häufigsten Arten, auf die dieser in Erscheinung tritt, sind Diabetes mellitus Typ 1 und Typ 2. Es gibt aber noch einen sog. Typ 3 und Typ 4.
Im Video gehe ich ausführlich auf die Zuckerkrankheit und die verschiedenen Typen ein.

Eine typische Patientengeschichte:
“In letzter Zeit fällt Thomas das Joggen zunehmend schwerer. Das Training verbessert seine Leistung nicht, es mindert sie! „Aber das kann doch nicht am Training liegen? Erstmal hinlegen, vielleicht wird’s dann besser“, denkt sich der Patient. Tatsächlich ist er seit kurzem öfter müde und gönnt sich deshalb das ein oder andere Mittagsschläfchen. Doch meist dauert dieses nicht lang, weil er häufiger dringend pinkeln muss und gleichzeitig enormen Durst hat.”

Bei Diabetes Mellitus handelt es sich um eine chronische Stoffwechselerkrankung mit absolutem bzw. relativem Insulinmangel sowie Hyperglykämie, also einer krankhaft erhöhten Menge Glukose im Blut.
Wenn wir Zucker zu uns nehmen, wird dieser normalerweise im Rahmen der Verdauung von den Darmepithelzellen aufgenommen. Von dort aus gelangt er ins Blut und kann mit Hilfe des Hormons Insulin in die Körperzellen befördert werden. In diesen wird der Zucker zur Gewinnung von Energie und der Synthese wichtiger Stoffwechselprodukte für den Körper genutzt. Das Insulin stammt dabei aus den B-Zellen der Bauchspeicheldrüse, des sog. Pankreas. Leidet man an Diabetes mellitus, ist dieser Weg gestört.

Die allgemeinen Symptome von Diabetes sind Müdigkeit und Leistungsminderung.
Hinzu kommt eine erhöhte Harnproduktion, die oberhalb von 2000 ml/Tag liegt (sog. ‚Polyurie‘). In der Folge hat der Patient oft ein quälendes Durstempfinden (sog. ‚Polydipsie‘).
Durch die Polyurie kommt es zur erhöhten Ausscheidung von Magnesium und Kalium, was wiederum Wadenkrämpfe verursachen kann und außerdem dafür verantwortlich ist, dass der Patient über trockene oder juckende Haut klagt, was vor allem durch den hohen Flüssigkeitsverlust verursacht wird.
Schwankungen im Blutzuckerspiegel können indes zu Sehstörungen führen und ein absoluter Mangel an Insulin kann Gewichtsabnahme zur Folge haben.

Wichtig: Viele dieser Symptome gehen vor allem mit Typ-1-Diabetes einher, während die Erkrankung bei Typ-2-Diabetikern anfangs eher asymptomatisch, also ohne erkennbare Symptome, verläuft.

Typische Folgen von Diabetes:
1. Diabetische Polyneuropathie (Nervenschädigungen)
2. Durchblutungsstörungen
3. Diabetische Retinopathie (Schädigung der Netzhaut)
4. Diabetische Nephropathie (Schädigung der Nieren)
5. Diabetischer Fuß (schlecht heilende Wunden am Fuß)

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Diabetes Type II Pathophysiology

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Diabetes Complication and Pathophysiology of the complication

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Diabetes mellitus series ( Part 1 ) – Types of Diabetes, Causes, Risk Factors, and Symptoms

Diabetes mellitus (DM) describes a group of metabolic diseases that are characterized by chronic hyperglycemia (elevated blood glucose levels). The two most common forms are type 1 and type 2 diabetes mellitus. Type 1 is the result of an autoimmune response that triggers the destruction of insulin-producing β cells in the pancreas and results in an absolute insulin deficiency. Type 2, which is much more common, has a strong genetic component as well as a significant association with obesity and sedentary lifestyles. Type 2 diabetes is characterized by insulin resistance (insufficient response of peripheral cells to insulin) and pancreatic β cell dysfunction (impaired insulin secretion), resulting in relative insulin deficiency. This form of diabetes usually remains clinically inapparent for many years. However, abnormal metabolism (prediabetic state or impaired glucose intolerance), which is associated with chronic hyperglycemia, causes microvascular and macrovascular changes that eventually result in cardiovascular, renal, retinal, and neurological complications. In addition, type 2 diabetic patients often present with other conditions (e.g. hypertension, dyslipidemia, obesity) that increase the risk of cardiovascular disease (e.g., myocardial infarction). Renal insufficiency is primarily responsible for the reduced life expectancy of patients with DM.
Because of the chronic, progressive nature of type 1 and type 2 diabetes mellitus, a comprehensive treatment approach is necessary. The primary treatment goals for type 2 diabetes are the normalization of glucose metabolism and the management of risk factors (e.g., arterial hypertension). In theory, weight normalization, physical activity, and a balanced diet should be sufficient to prevent the manifestation of diabetes in prediabetic patients or delay the progression of disease in diabetic patients. Unfortunately, these general measures alone are rarely successful, and treatment with oral antidiabetic drugs and/or insulin injections is often required for optimal glycemic control. In type 1 diabetes, insulin replacement therapy is essential and patients must learn to coordinate insulin injections and dietary carbohydrates. Both type 1 and type 2 diabetic patients require regular self-management training to improve glycemic control, reduce the risk of life-threatening hypoglycemia or hyperglycemia, and prevent diabetic complications.

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Pathophysiology of Diabetes Mellitus

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Description of pathophysiology of type 1 and type 2 diabetes, and a discussion of complications.
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Diabetes Mellitus Pathophysiology & Nursing | Diabetes Nursing Lecture NCLEX | Type 1 & Type 2

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Diabetes mellitus pathophysiology and nursing nclex lecture review on diabetes type 1 and diabetes type 2. Diabetes mellitus is where a patient has insufficient amounts of insulin to use the blood glucose in the body. Therefore, the patient will experience extreme hyperglycemica. In this lecture, I highlight the key players in diabetes mellitus, causes, different types of diabetes (type 1, type 2, and gestational), complications, and nursing assessment of the diabetic patient.

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