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Why Do Ketone Bodies Cause Acidosis?

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DKA diabetic ketoacidosis nursing management pathophysiology & treatment. DKA is a complication of diabetes mellitus and mainly affects type 1 diabetics. DKA management includes controlling hyperglycemia, ketosis, and acdidosis. Signs & Symptoms include polyuria, polydipsia, hyperglycemia greater than 300 mg/dL, Kussmaul breathing, acetone breath, and ketones in the urine. Typically DKA treatment includes: intravenous fluids, insulin therapy (IV regular insulin), and electrolyte replacement. This video details what the nurse needs to know for the NCLEX exam about diabetic ketoacidosis. I also touch on DKA vs HHS (diabetic ketoacidosis and hyperosmolar hyperglycemic nonketotic syndrome (please see the other video for more details). Quiz on DKA: http://www.registerednursern.com/diab... Lecture Notes for this video: http://www.registerednursern.com/diab... Diabetes NCLEX Review Videos: https://www.youtube.com/playlist?list... 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

Diabetic Ketoacidosis (dka)

A 12 year old boy, previously healthy, is admitted to the hospital after 2 days of polyuria, polyphagia, nausea, vomiting and abdominal pain. Vital signs are: Temp 37C, BP 103/63 mmHg, HR 112, RR 30. Physical exam shows a lethargic boy. Labs are notable forWBC 16,000,Glucose 534, K 5.9, pH 7.13, PCO2 is 20 mmHg, PO2 is 90 mmHg. result of insulin, glucagon, growth hormone, catecholamine increased tidal volume and rate as a result of metabolic acidosis due to gluconeogenesis and glycogenolysis tissues unable to use the high glucose as it is unable to enter cells anion gap due to ketoacidosis, lactic acidosis consumed in an attempt to buffer the increased acid glucose acts as an osmotic agent and draws water from ICF to ECF acidosis results in ICF/ECF exchange of H+ for K+ depletion of total body potassium due to cellular shift and losses through urine -hydroxybutyrate not detected with normal ketone body tests due to in capillary lipoprotein lipase activity H2PO4- is increased in urine, as it is titratable acid used to buffer the excess H+ that is being excreted must prevent resultant hypokalemia and hypophosphatemia labs may show pseudo-hyperkalemia prior to administartion of fluid Continue reading >>

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  1. * DKA explanation

    * DKA explanation

    Below you will find a terrific explanation of DKA from one of the instructors at Med School Tutors. If you like what you see and may be interested in learning more about one-on-one instruction from MST, then please visit their website at www.medschooltutors.com
    In order to understand how to treat DKA, it is useful to first understand what is going on in the body when DKA develops. First of all, DKA (diabetic ketoacidosis) typically develops when a Type I diabetic does not take his or her insulin for a prolonged period of time. It may also be the presentation for new onset diabetes. Because these patients are insulin deficient, they are not able to take up glucose into their cells. This results in two important consequences: 1)glucose builds up in the blood and causes hyperglycemia and 2)the body's cells are forced to breakdown fat for energy, instead of glucose.
    These are very significant consequences... The hyperglycemia results in an osmotic diuresis, because the proximal tubule of the kidney can't reabsorb all the glucose filtered into the nephron. What is osmotic diuresis? Simply that the hyperglycemia (usually >300) causes the body to excrete lots and lots of water, because the osmotic pull of all the glucose particles prevents the reabsorbtion of water in the collecting duct. This means that patients with DKA are peeing their brains out!! They pee out sodium, potassium, and water.. And are therefore, very very very DEHYDRATED, sodium depleted, and potassium depleted.
    Now for the metabolism end of things... The body cells are forced to metabolize fat for energy rather than glucose. How do they accomplish this? - beta-oxidation of fatty acids. This results in excess production of ketone bodies which deplete available acid buffers. This causes a significant metabolic acidosis, with a high anion gap due to the presence of ketoacids. The acidosis causes potassium to shift from the intracellular space to the extracellular space. This may result in a normal or high serum potassium level. This normal or high potassium level masks what is typically significant potassium depletion because the person was peeing all their potassium out as a result of the uncontrolled hyperglycemia.
    So what are we going to do now? I will give a very brief answer for now, expect people to ask questions in the meantime, and then provide a more thorough approach to treatment in the coming days.
    1)Give the patient tons of normal saline. Why? - because your patient is dehydrated as all hell. They have been peeing out every last drop of water because of their severe uncontrolled hyperglycemia. These patients require liters of fluid to replenish all the fluid they've lost as a result of the osmotic diuresis.
    2)Give them insulin. Why? - NOT because it will lower the blood glucose level, but because it will cause a shift away from fat metabolism and toward glucose metabolism. This will slow the production of ketone bodies which are precipitating the metabolic acidosis. Thus, I will repeat, we give insulin to shift away from fat metabolism and stop the production of ketone bodies.
    3)Give the patient potassium. Why? - As we discussed earlier, the person has been peeing out all of their potassium stores and are overall very potassium depleted, despite having normal or high serum potassium levels to begin with. In addition to being potassium depleted, the insulin you are giving will cause a shift of potassium from the extracellular space to the intracellular space, which will drop the serum potassium. Thus, we give DKA patients potassium way before they become hypokalemic.
    4)Give the patient dextrose. Why? - They insulin you are giving the patient is obviously going to cause the serum glucose to decrease. We give glucose to prevent hypoglycemia as we continue to give insulin.
    How do we know when we are finished treating these patients? - When the anion gap returns to normal.
    That's all for now. Please ask any questions you have. I will be giving more specifics about DKA management in the near future.
    PS: Does anyone know the dangerous consequence of giving DKA patients fluid too rapidly? What are the symptoms this may cause, and what is the pathophysiology behind these symptoms?

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Understand medical acid base problems with this clear explanation from Dr. Seheult of http://www.medcram.com. This is video 2 of 8 on medical acid base. Speaker: Roger Seheult, MD Clinical and Exam Preparation Instructor Board Certified in Internal Medicine, Pulmonary Disease, Critical Care, and Sleep Medicine. Co-founder of http://www.medcram.com. MedCram: Medical topics explained clearly including: Asthma, COPD, Acute Renal Failure, Mechanical Ventilation, Oxygen Hemoglobin Dissociation Curve, Hypertension, Shock, Diabetic Ketoacidosis (DKA), Medical Acid Base, VQ Mismatch, Hyponatremia, Liver Function Tests, Pulmonary Function Tests (PFTs), Adrenal Gland, Pneumonia Treatment, any many others. New topics are often added weekly- please subscribe to help support MedCram and become notified when new videos have been uploaded. Subscribe: https://www.youtube.com/subscription_... Recommended Audience: Health care professionals and medical students: including physicians, nurse practitioners, physician assistants, nurses, respiratory therapists, EMT and paramedics, and many others. Review for USMLE, MCAT, PANCE, NCLEX, NAPLEX, NDBE, RN, RT, MD, DO, PA, NP school and board examinations. M

Medcram Medical Education Blog

Were gonna talk about diabetic ketoacidosis DKA. DKA is a pretty significant illness that accounts for about 135.000 hospital admissions every year in the United States and it has an estimated cost of about 2.4 billion US dollars every year. So, a pretty sizeable chunk of cash is used to treat these patients and so, it behooves us to understand a little bit more about what is DKA, how does it present and how to treat it. First, I want to take you to the cellular level. Over here, I will show you our cell wall and on it, its got an insulin receptor. Also, inside the cell, you recall that we have mitochondria and youll recall that there is an inner-membrane space, along with the matrix. The matrix is that inner part. Now, remember where things are. Youve got glucose outside the cell, that wants to move inside, and youve got fatty acids as well. Well draw a fatty acid here. You recall that this is where Krebs cycle occurs; Ill abbreviate that as KC. This is where you have beta-oxidation. Remember these? Fatty acids move inside the cell. Youll also recall that glucose, once it gets inside the cell, is going to undergo glycolysis and it will also go inside the cell in the form of pyruv Continue reading >>

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  1. Knicks

    In DKA, the patient is acidotic, right? So why would the body decrease bicarbonate (a base)? Wouldn't you want to keep the bicarbonate high so as to neutralize the acid?
    Too tired to think straight at the moment.

  2. generic

    The HCO3 derangement is not a compensation--it is the primary problem.
    DKA patients have a metabolic acidosis, I think it's mostly caused by the formation of tons and tons of ketone bodies (acidic). These are formed because despite high circulating levels of glucose, the cells can't use the glucose without insulin-->turn to ketone formation instead.
    The metabolic acidosis may cause respiratory compensation, which would give Kussmaul breathing, for example.

  3. treva

    Knicks said: ↑
    In DKA, the patient is acidotic, right? So why would the body decrease bicarbonate (a base)? Wouldn't you want to keep the bicarbonate high so as to neutralize the acid?
    Too tired to think straight at the moment. Remember the kidney takes days to compensate for acidodic state by producing more bicarb. Acutely, the bicarb is used to buffer the extra acid, so it drops.
    This also explains why DKA pts have increased RR:
    CO2 + H20 <--> H2CO3 <--> HCO3- + H+
    If you blow off extra CO2 (ie by upping RR) you shift the above equation to the left, and promote the formation of H2CO3 via CA, helping to mop up the H+.

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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 b

The Pathophysiology Of Diabetic Ketoacidosis

People still die from diabetic ketoacidosis. Poor patient education is probably the mostimportant determinant of the incidence of the catastrophe that constitutes "DKA".In several series, only about a fifth of patients with DKA are first-time presenterswith recently acquired Type I diabetes mellitus. The remainder are recognised diabeticswho are either noncompliant with insulin therapy, or have serious underlying illess thatprecipitates DKA. Most such patients have type I ("insulin dependent", "juvenile onset") diabetes mellitus, but it has recently been increasingly recognised that patients with type II diabetes mellitusmay present with ketoacidosis, and that some such patients present with "typical hyperosmolar nonketotic coma", but on closer inspection have varying degrees of ketoacidosis. DKA is best seen as a disorder that follows on an imbalance between insulin levels andlevels of counterregulatory hormones. Put simply: "Diabetic ketoacidosis is due to a marked deficiency of insulin in the face of high levels of hormones thatoppose the effects of insulin, particularly glucagon. Even small amounts of insulin can turn off ketoacid formation". Many hormones antagonise the effec Continue reading >>

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Popular Questions

  1. Knicks

    In DKA, the patient is acidotic, right? So why would the body decrease bicarbonate (a base)? Wouldn't you want to keep the bicarbonate high so as to neutralize the acid?
    Too tired to think straight at the moment.

  2. generic

    The HCO3 derangement is not a compensation--it is the primary problem.
    DKA patients have a metabolic acidosis, I think it's mostly caused by the formation of tons and tons of ketone bodies (acidic). These are formed because despite high circulating levels of glucose, the cells can't use the glucose without insulin-->turn to ketone formation instead.
    The metabolic acidosis may cause respiratory compensation, which would give Kussmaul breathing, for example.

  3. treva

    Knicks said: ↑
    In DKA, the patient is acidotic, right? So why would the body decrease bicarbonate (a base)? Wouldn't you want to keep the bicarbonate high so as to neutralize the acid?
    Too tired to think straight at the moment. Remember the kidney takes days to compensate for acidodic state by producing more bicarb. Acutely, the bicarb is used to buffer the extra acid, so it drops.
    This also explains why DKA pts have increased RR:
    CO2 + H20 <--> H2CO3 <--> HCO3- + H+
    If you blow off extra CO2 (ie by upping RR) you shift the above equation to the left, and promote the formation of H2CO3 via CA, helping to mop up the H+.

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