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Dka Pathophysiology Diagram

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DKA and HHS (HHNS) nursing NCLEX lecture review of the treatment, patient signs/symptoms, and management. Diabetic ketoacidosis and hyperosmolar hyperglycemia nonketotic syndrome are two complications that can present in diabetes mellitus. DKA is more common in type 1 diabetics, whereas, HHNS is more common in type 2 diabetics. Patients with diabetic ketoacidosis will present with ketosis and acidosis and signs/symptoms will include hyperglycemia (greater than 300 mg/dL), Kussmaul breathing, fruity (acetone breath), ketones in the urine, and metabolic acidosis. Patients with hyperglycemic hyperosmolar syndrome will NOT have ketosis or acidosis but EXTREME hyperglycemia (greater than 600 mg/dL). In addition, hyperosmolarity will present which will cause major osmotic diuresis and the patient will experience with severe dehydration. Quiz on DKA vs HHNS: http://www.registerednursern.com/dka-... Lecture Notes for this video: http://www.registerednursern.com/dka-... Diabetes NCLEX Review Series: https://www.youtube.com/playlist?list... Video on DKA (detailed lecture): https://www.youtube.com/watch?v=IxrCV... Video on HHNS (detailed lecture): https://www.youtube.com/watch?v=LyExA... Subscribe: http://www.youtube.com/subscription_c... Nursing School Supplies: http://www.registerednursern.com/the-... Nursing Job Search: http://www.registerednursern.com/nurs... Visit our website RegisteredNurseRN.com for free quizzes, nursing care plans, salary information, job search, and much more: http://www.registerednursern.com Check out other Videos: https://www.youtube.com/user/Register... Popular Playlists: "NCLEX Study Strategies": https://www.youtube.com/playlist?list... "Fluid & Electrolytes Made So Easy": https://www.youtube.com/playlist?list... "Nursing Skills Videos": https://www.youtube.com/playlist?list... "Nursing School Study Tips": https://www.youtube.com/playlist?list... "Nursing School Tips & Questions": https://www.youtube.com/playlist?list... "Teaching Tutorials": https://www.youtube.com/playlist?list... "Types of Nursing Specialties": https://www.youtube.com/playlist?list... "Healthcare Salary Information": https://www.youtube.com/playlist?list... "New Nurse Tips": https://www.youtube.com/playlist?list... "Nursing Career Help": https://www.youtube.com/playlist?list... "EKG Teaching Tutorials": https://www.youtube.com/playlist?list... "Personality Types": https://www.youtube.com/playlist?list... "Dosage & Calculations for Nurses": https://www.youtube.com/playlist?list... "Diabetes Health Managment": https://www.youtube.com/playlist?list...

Dka Vs Hhs (hhns) Nclex Review

Diabetic ketoacidosis vs hyperglycemic hyperosmolar nonketotic syndrome (HHNS or HHS): What are the differences between these two complications of diabetes mellitus? This NCLEX review will simplify the differences between DKA and HHNS and give you a video lecture that easily explains their differences. Many students get these two complications confused due to their similarities, but there are major differences between these two complications. After reviewing this NCLEX review, don’t forget to take the quiz on DKA vs HHNS. Lecture on DKA and HHS DKA vs HHNS Diabetic Ketoacidosis Affects mainly Type 1 diabetics Ketones and Acidosis present Hyperglycemia presents >300 mg/dL Variable osmolality Happens Suddenly Causes: no insulin present in the body or illness/infection Seen in young or undiagnosed diabetics Main problems are hyperglycemia, ketones, and acidosis (blood pH <7.35) Clinical signs/symptoms: Kussmaul breathing, fruity breath, abdominal pain Treatment is the same as in HHNS (fluids, electrolyte replacement, and insulin) Watch potassium levels closely when giving insulin and make sure the level is at least 3.3 before administrating. Hyperglycemic Hyperosmolar Nonketotic Syn Continue reading >>

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  1. NicoleAnn

    Ketones and Unrinary Tract Infection

    Is it normal when you have a high level of ketone's in your system to get a urinary tract infection? I'm kinda wondering about it, since my doctor doesn't listen to me when I say I have ketone's and he gives me antibiotics for a urinary tract infection. Any help would be greatly appreciated.

  2. MarkM

    Infections are not caused by ketones. But they are encouraged by the high blood sugar that often accompanies ketones. Bacteria love warm moist places where there are lots of nutrients. If you lower your blood sugar to the point there is no longer sugar in your urine, you will be removing one of the key attractions. And hopefully you won't get so many infections. But until this happens, you are going to have to use antibiotics ... .

  3. Kaki

    I already commented on your blog this morning regarding ketones, as an individual who has had many UTI's, women know when they have an infection, as its not possible to urinate without that burning sensation, which we do not tolerate very well and will send you immediately to your doctor for medication to resolve a UTI, you made no mention as to whether you did in fact give your doctor a urine specimen.

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What is DIABETIC KETOACIDOSIS? What does DIABETIC KETOACIDOSIS mean? DIABETIC KETOACIDOSIS meaning - DIABETIC KETOACIDOSIS definition - DIABETIC KETOACIDOSIS explanation. Source: Wikipedia.org article, adapted under https://creativecommons.org/licenses/... license. SUBSCRIBE to our Google Earth flights channel - https://www.youtube.com/channel/UC6Uu... Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes mellitus. Signs and symptoms may include vomiting, abdominal pain, deep gasping breathing, increased urination, weakness, confusion, and occasionally loss of consciousness. A person's breath may develop a specific smell. Onset of symptoms is usually rapid. In some cases people may not realize they previously had diabetes. DKA happens most often in those with type 1 diabetes, but can also occur in those with other types of diabetes under certain circumstances. Triggers may include infection, not taking insulin correctly, stroke, and certain medications such as steroids. DKA results from a shortage of insulin; in response the body switches to burning fatty acids which produces acidic ketone bodies. DKA is typically diagnosed when testing finds high blood sugar, low blood pH, and ketoacids in either the blood or urine. The primary treatment of DKA is with intravenous fluids and insulin. Depending on the severity, insulin may be given intravenously or by injection under the skin. Usually potassium is also needed to prevent the development of low blood potassium. Throughout treatment blood sugar and potassium levels should be regularly checked. Antibiotics may be required in those with an underlying infection. In those with severely low blood pH, sodium bicarbonate may be given; however, its use is of unclear benefit and typically not recommended. Rates of DKA vary around the world. About 4% of people with type 1 diabetes in United Kingdom develop DKA a year, while in Malaysia the condition affects about 25% a year. DKA was first described in 1886 and, until the introduction of insulin therapy in the 1920s, it was almost universally fatal. The risk of death with adequate and timely treatment is currently around 1–4%. Up to 1% of children with DKA develop a complication known as cerebral edema. The symptoms of an episode of diabetic ketoacidosis usually evolve over a period of about 24 hours. Predominant symptoms are nausea and vomiting, pronounced thirst, excessive urine production and abdominal pain that may be severe. Those who measure their glucose levels themselves may notice hyperglycemia (high blood sugar levels). In severe DKA, breathing becomes labored and of a deep, gasping character (a state referred to as "Kussmaul respiration"). The abdomen may be tender to the point that an acute abdomen may be suspected, such as acute pancreatitis, appendicitis or gastrointestinal perforation. Coffee ground vomiting (vomiting of altered blood) occurs in a minority of people; this tends to originate from erosion of the esophagus. In severe DKA, there may be confusion, lethargy, stupor or even coma (a marked decrease in the level of consciousness). On physical examination there is usually clinical evidence of dehydration, such as a dry mouth and decreased skin turgor. If the dehydration is profound enough to cause a decrease in the circulating blood volume, tachycardia (a fast heart rate) and low blood pressure may be observed. Often, a "ketotic" odor is present, which is often described as "fruity", often compared to the smell of pear drops whose scent is a ketone. If Kussmaul respiration is present, this is reflected in an increased respiratory rate.....

Diabetic Ketoacidosis

Professor of Pediatric Endocrinology University of Khartoum, Sudan Introduction DKA is a serious acute complications of Diabetes Mellitus. It carries significant risk of death and/or morbidity especially with delayed treatment. The prognosis of DKA is worse in the extremes of age, with a mortality rates of 5-10%. With the new advances of therapy, DKA mortality decreases to > 2%. Before discovery and use of Insulin (1922) the mortality was 100%. Epidemiology DKA is reported in 2-5% of known type 1 diabetic patients in industrialized countries, while it occurs in 35-40% of such patients in Africa. DKA at the time of first diagnosis of diabetes mellitus is reported in only 2-3% in western Europe, but is seen in 95% of diabetic children in Sudan. Similar results were reported from other African countries . Consequences The latter observation is annoying because it implies the following: The late diagnosis of type 1 diabetes in many developing countries particularly in Africa. The late presentation of DKA, which is associated with risk of morbidity & mortality Death of young children with DKA undiagnosed or wrongly diagnosed as malaria or meningitis. Pathophysiology Secondary to insulin Continue reading >>

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  1. Hot Flashes

    Happened to me too

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Respiratory acidosis #sign and symptoms of Respiratory acidosis Respiratory acidosis ABGs Analyse https://youtu.be/L5MWy1iHacI Plz share n subscribe my chanel is a condition that occurs when the lungs cant remove enough of the Suctioning https://youtu.be/hMJGkxvXTW0 carbon dioxide (CO2) produced by the body. Excess CO2 causes the pH of blood and other bodily fluids to decrease, making them too acidic. Normally, the body is able to balance the ions that control acidity. This balance is measured on a pH scale from 0 to 14. Acidosis occurs when the pH of the blood falls below 7.35 (normal blood pH is between 7.35 and 7.45).Rinku Chaudhary NSG officer AMU ALIGARH https://www.facebook.com/rinkutch/ Respiratory acidosis is typically caused by an underlying disease or condition. This is also called respiratory failure or ventilatory failure. Suctioning https://youtu.be/hMJGkxvXTW0 Normally, the lungs take in oxygen and exhale CO2. Oxygen passes from the lungs into the blood. CO2 passes from the blood into the lungs. However, sometimes the lungs cant remove enough CO2. This may be due to a decrease in respiratory rate or decrease in air movement due to an underlying condition such as: asthma COPD pneumonia sleep apnea TYPES Forms of respiratory acidosis There are two forms of respiratory acidosis: acute and chronic. Acute respiratory acidosis occurs quickly. Its a medical emergency. Left untreated, symptoms will get progressively worse. It can become life-threatening. Chronic respiratory acidosis develops over time. It doesnt cause symptoms. Instead, the body adapts to the increased acidity. For example, the kidneys produce more bicarbonate to help maintain balance. Chronic respiratory acidosis may not cause symptoms. Developing another illness may cause chronic respiratory acidosis to worsen and become acute respiratory acidosis. SYMPTOMS Symptoms of respiratory acidosis Initial signs of acute respiratory acidosis include: headache anxiety blurred vision restlessness confusion Without treatment, other symptoms may occur. These include: https://www.healthline.com/health/res... sleepiness or fatigue lethargy delirium or confusion shortness of breath coma The chronic form of respiratory acidosis doesnt typically cause any noticeable symptoms. Signs are subtle and nonspecific and may include: memory loss sleep disturbances personality changes CAUSES Common causes of respiratory acidosis The lungs and the kidneys are the major organs that help regulate your bloods pH. The lungs remove acid by exhaling CO2, and the kidneys excrete acids through the urine. The kidneys also regulate your bloods concentration of bicarbonate (a base). Respiratory acidosis is usually caused by a lung disease or condition that affects normal breathing or impairs the lungs ability to remove CO2. Some common causes of the chronic form are: asthma chronic obstructive pulmonary disease (COPD) acute pulmonary edema severe obesity (which can interfere with expansion of the lungs) neuromuscular disorders (such as multiple sclerosis or muscular dystrophy) scoliosis Some common causes of the acute form are: lung disorders (COPD, emphysema, asthma, pneumonia) conditions that affect the rate of breathing muscle weakness that affects breathing or taking a deep breath obstructed airways (due to choking or other causes) sedative overdose cardiac arrest DIAGNOSIS How is respiratory acidosis diagnosed? The goal of diagnostic tests for respiratory acidosis is to look for any pH imbalance, to determine the severity of the imbalance, and to determine the condition causing the imbalance. Several tools can help doctors diagnose respiratory acidosis. Blood gas measurement Blood gas is a series of tests used to measure oxygen and CO2 in the blood. A healthcare provider will take a sample of blood from your artery. High levels of CO2 can indicate acidosis.

Respiratory Failure In Diabetic Ketoacidosis

Go to: INTRODUCTION Ketoacidosis in subjects with type 1, or less frequently, type 2 diabetes mellitus remains a potentially life-threatening diabetic manifestation. The subject has justifiably attracted attention in the literature. Sequential reviews[1-9] have documented important changes in the clinical concepts that are related to diabetic ketoacidosis (DKA) and its management. A large number of case series of DKA have addressed various aspects of its clinical presentation and management. For this review, we selected representative studies focused on management, outcome, age differences, gender differences, associated morbid conditions, ethnicity and prominent clinical and laboratory features[10-35]. In recognition of the complexity of treatment, the recommendation to provide this care in intensive care units was made more than 50 years ago[36]. Severe DKA is treated in intensive care units today[31]. Evidence-based guidelines for the diagnosis and management of DKA have been published and frequently revised in North America[37,38] and Europe[39]. Losses of fluids and electrolytes, which are important causes of morbidity and mortality in DKA, vary greatly between patients. Quant Continue reading >>

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  1. manohman

    Why can't fat be converted into Glucose?

    So the reason cited is that beta oxidation/metabolism of fats leads to formation of acetyl coa, a 2 carbon molecule, and that because of that it cannot be converted back into glucose.
    Why exactly is that the case?
    If Glucogenic amino acids can be converted into citric acid cycle intermediates and then turn back into glucose via gluconeogensis, then why cant Fatty Acids which yield Acetyl Coa. Can't you just have Acetyl Coa enter the citric acid cycle and produce the same intermediates that the glucogenic amino acids creat?

  2. Czarcasm

    manohman said: ↑
    So the reason cited is that beta oxidation/metabolism of fats leads to formation of acetyl coa, a 2 carbon molecule, and that because of that it cannot be converted back into glucose.
    Why exactly is that the case?
    If Glucogenic amino acids can be converted into citric acid cycle intermediates and then turn back into glucose via gluconeogensis, then why cant Fatty Acids which yield Acetyl Coa. Can't you just have Acetyl Coa enter the citric acid cycle and produce the same intermediates that the glucogenic amino acids creat?
    Click to expand... Both glucose and fatty acids can be stored in the body as either glycogen for glucose (stored mainly in the liver or skeletal cells) or for FA's, as triacylglycerides (stored in adipose cells). We cannot store excess protein. It's either used to make other proteins, or flushed out of the body if in excess; that's generally the case but we try to make use of some of that energy instead of throwing it all away.
    When a person is deprived of nutrition for a period of time and glycogen stores are depleted, the body will immediately seek out alternative energy sources. Fats (stored for use) are the first priority over protein (which requires the breakdown of tissues such as muscle). We can mobilize these FA's to the liver and convert them to Acetyl-CoA to be used in the TCA cycle and generate much needed energy. On the contrary, when a person eats in excess (a fatty meal high in protein), it's more efficient to store fatty acids as TAG's over glycogen simply because glycogen is extremely hydrophilic and attracts excess water weight; fatty acids are largely stored anhydrously and so you essentially get more bang for your buck. This is evolutionary significant and why birds are able to stay light weight but fly for periods at a time, or why bears are able to hibernate for months at a time. Proteins on the other hand may be used anabolically to build up active tissues (such as when your working out those muscles), unless you live a sedentary lifestyle (less anabolism and therefore, less use of the proteins). As part of the excretion process, protein must be broken down to urea to avoid toxic ammonia and in doing so, the Liver can extract some of that usable energy for storage as glycogen.
    Also, it is worth noting that it is indeed possible to convert FA's to glucose but the pathway can be a little complex and so in terms of energy storage, is not very efficient. The process involves converting Acetyl-CoA to Acetone (transported out of mitochondria to cytosol) where it's converted to Pyruvate which can then be used in the Gluconeogenesis pathway to make Glucose and eventually stored as Glycogen. Have a look for yourself if your interested: http://www.ploscompbiol.org/article/info:doi/10.1371/journal.pcbi.1002116.g003/originalimage (and this excludes the whole glycogenesis pathway, which hasn't even begun yet).
    TLDR: it's because proteins have no ability to be stored in the body, but we can convert them to glycogen for storage during the breakdown process for excretion. Also, in terms of energy, it's a more efficient process than converting FA's to glycogen for storage.

  3. soccerman93

    This is where biochem comes in handy. Czarcasm gives a really good in depth answer, but a simpler approach is to count carbons. The first step of gluconeogenesis(formation of glucose) requires pyruvate, a 3 carbon molecule. Acetyl Co-A is a 2 carbon molecule, and most animals lack the enzymes (malate synthase and isocitrate lyase) required to convert acetyl co-A into a 3 carbon molecule suitable for the gluconeogenesis pathway. The ketogenic pathway is not efficient, as czarcasm pointed out. While acetyl co-A can indeed be used to form citric acid intermediates, these intermediates will be used in forming ATP, not glucose. Fatty acid oxidation does not yield suitable amounts of pyruvate, which is required for gluconeogenesis. This is part of why losing weight is fairly difficult for those that are overweight, we can't efficiently directly convert fat to glucose, which we need a fairly constant supply of. Sorry, that got a little long-winded

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