diabetestalk.net

Dka Potassium Usmle

Archive Of Standardized Exam Questions: Diabetic Ketoacidosis (dka)

Archive Of Standardized Exam Questions: Diabetic Ketoacidosis (dka)

This page is dedicated to organizing various examples of standardized exam questions whose answer is diabetic ketoacidosis (DKA) .While this may seem a odd practice, it is useful to see multipleexamples of how DKA will be characterized on standardized exams (namely the boards and the shelf exams). This page is not meant to be used as a tradition question bank (as all of the answers will be the same), however seeing the classic test characterization for a disease is quite valuable. KEY CHARACTERISTICS OF THIS CONDITION (ON EXAMS) When it comes to standardized exams, each topichas its own code marked by key buzzwords, lab findings, clues, etc. If you are well versed in this code you will be able to more quickly identify the condition that is being discussed, and get the right answer on the exam you are taking. Below is the code for DKA . Diagnosis of diabetes:generally more common in type 1 diabetes Symptomssuggestive of diabetes:urinary frequency and thirst can hint at a diagnosis of type 1 diabetes . Fruity odor on breathis a very specific clue Rapidbreathing :Kussmaul respirationsare classically seen Diffuseabdominaltenderness:especially to deep palpation Decreased blood pH:patients will have acidemia Ketones in urine/serum:required for the real-life diagnosis Hyperkalemiawill also be present in patients (due to lack of insulin driving it into cells). A 10 year old girl is brought to the hospital because she has fatigue, difficultybreathing, and has also been having many episodes of vomiting today. Her skin is flushed, warm, and she appears to be volume depleted. There is afruity odor noted when smelling her breath. She is in the 80th percentile for height, and the 25th percentile for weight. Her temperature 99.2F, pulse is 115/min, respirations are 25/min, and blood Continue reading >>

Understanding The Presentation Of Diabetic Ketoacidosis

Understanding The Presentation Of Diabetic Ketoacidosis

Hypoglycemia, diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar nonketotic syndrome (HHNS) must be considered while forming a differential diagnosis when assessing and managing a patient with an altered mental status. This is especially true if the patient has a history of diabetes mellitus (DM). However, be aware that the onset of DKA or HHNS may be the first sign of DM in a patient with no known history. Thus, it is imperative to obtain a blood glucose reading on any patient with an altered mental status, especially if the patient appears to be dehydrated, regardless of a positive or negative history of DM. In addition to the blood glucose reading, the history — particularly onset — and physical assessment findings will contribute to the formulation of a differential diagnosis and the appropriate emergency management of the patient. Pathophysiology of DKA The patient experiencing DKA presents significantly different from one who is hypoglycemic. This is due to the variation in the pathology of the condition. Like hypoglycemia, by understanding the basic pathophysiology of DKA, there is no need to memorize signs and symptoms in order to recognize and differentiate between hypoglycemia and DKA. Unlike hypoglycemia, where the insulin level is in excess and the blood glucose level is extremely low, DKA is associated with a relative or absolute insulin deficiency and a severely elevated blood glucose level, typically greater than 300 mg/dL. Due to the lack of insulin, tissue such as muscle, fat and the liver are unable to take up glucose. Even though the blood has an extremely elevated amount of circulating glucose, the cells are basically starving. Because the blood brain barrier does not require insulin for glucose to diffuse across, the brain cells are rece Continue reading >>

Role Of Insulin In Diabetic Ketoacidosis

Role Of Insulin In Diabetic Ketoacidosis

Answer- The right answer is- c) Glucose transport in muscle. The child is suffering from diabetic ketoacidosis, the commonest complication of Type 1 diabetes mellitus. Fruity odor of breath is due to the presence of acetone, one of the ketone bodies (the other two are acetoacetate and beta hydroxy butyrate). Acetone is excreted through lungs. High blood glucose is due to non utilization or extra synthesis of glucose in the presence of reversed insulin to glucagon ratio. In the conditions of non utilization of glucose, fats are alternatively oxidized to provide energy. The extra Acetyl co A produced by fatty acid oxidation is diverted to the pathway of ketogenesis. Insulin does not promote gluconeogenesis, rather it inhibits it. Similarly fatty acid release from adipose tissue (adipolysis) is an action of glucagon and catecholamines, insulin inhibits this action also. Ketone utilization in brain is also not the correct option. By promoting glucose utilization, insulin inhibits ketosis; in fact ketosis occurs only when glucose is not available for utilization as in starvation, low carbohydrate/high fat diet, or diabetes mellitus. Glycogenolysis is also not the correct answer. Insulin promotes glycogenesis, it is an anabolic hormone, and it prevents all the catabolic processes including glycogenolysis. In diabetic ketoacidosis, Insulin promotes glucose uptake through GLUT4 transporters (figure) in skeletal, cardiac muscle and adipose tissue. It also promotes glucose utilization by stimulating the enzymes of pathways of glucose utilization. IV fluids are given to treat dehydration as DKA is mostly associated with polyuria. Potassium chloride is given to maintain potassium balance. Figure- Insulin increases the number of GLUT4 transporters present on the surface of adipose, Continue reading >>

Hypomagnesemia - Wikipedia

Hypomagnesemia - Wikipedia

This article is about the blood condition. For the general condition, see Magnesium deficiency (medicine) . For the condition in plants, see Magnesium deficiency (plants) . Hypomagnesemia, also spelled hypomagnesaemia, is an electrolyte disturbance in which there is a low level of magnesium in the blood. [1] Normal magnesium levels are between 1.462.68mg/dL (0.6-1.1 mmol/L) with levels less than 1.46mg/dL (0.6mmol/L) defining hypomagnesemia. [2] Symptoms include tremor, nystagmus , seizures , and cardiac arrest including torsade de pointes . [2] Causes include alcoholism , starvation , diarrhea , increased urinary loss, and poor absorption from the intestines . [2] Hypomagnesemia is not necessarily magnesium deficiency . Specific electrocardiogram (ECG) changes may be seen. [2] For those with severe disease intravenous magnesium sulfate may be used. [2] The prefix hypo- means under (contrast with hyper-, meaning over). The root 'magnes' refers to magnesium. The suffix of the word, -emia, means 'in the blood'. Deficiency of magnesium can cause tiredness, generalized weakness, muscle cramps, abnormal heart rhythms , increased irritability of the nervous system with tremors , paresthesias , palpitations , hypokalemia , hypoparathyroidism which might result in hypocalcemia , chondrocalcinosis , spasticity and tetany , epileptic seizures , basal ganglia calcifications and in extreme and prolonged cases coma , intellectual disability or death. [3] Other symptoms that have been suggested to be associated with hypomagnesemia are athetosis , jerking, nystagmus , and an extensor plantar reflex , confusion, disorientation, hallucinations , depression , hypertension and fast heart rate .[ citation needed ] People being treated on an intensive care unit who have a low magnesium lev Continue reading >>

Diabetic Ketoacidosis (dka)

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 and insulin due to transcellular shift of potassium out of the cells to balance the H+ being transfered into the cells Upon administration of insulin, potassium will shift intracellularly, possibly resulting in dangerous hypokalemia give phosphatesupplementation to prevent respiratory paralysis (M1.EC.31) A 17-year-old male presents to your office complaining of polyuria, polydipsia, and unintentional weight loss of 12 pounds over the past 3 months. On physical examination, the patient is tachypneic with labored breathing. Which of the following electrolyte abnormalities would you most likely Continue reading >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

 A 12 year old boy, previously healthy, is admitted to the hospiral after 2 days of polyuria, polyphagia, nausea, vomting and abdominal pain. Temp is 37, BP 103/63, HR 112, RR 30. Physical exam shows a lethargic boy.  Glucose is 534, Potasium is 5.9; WBC 16,000, pH is 7.13, PCO2 is 20 mmHg, PO2 is 90 mmHg. surge in counterregulatory homones (glucagon, growth hormone, catecholamine) Kussmaul Respiration (increased tidal volume)  associated with high mortality in pediatric patients expect to see an increase in free calcium since the excess hydrogen displaces calcium from albumin  give insulin until ketones are gone, even after glucose normalizes or is below normal caused by too much potassium being secreted in the urine as a result of the glucosuria due to transcellular shift of potassium out of the cells to balance the H being transfered into the cells  give in the form of potassium phosphate rather than potasium chloride give phosphate supplementation to prevent respiratory paralysis If mental status changes (headache, obtundation, coma) occur during treatment (M2.EC.2) A 19-year-old male presents to the emergency room with altered mental status. History is remarkable for increased urination over the past few months. On physical examination, he is a thin, young man with labored breathing, abdominal tenderness, and mild flank pain. Temperature is 37.0 degrees Celsius. An arterial blood gas shows serum pH 7.05, pCO2 17, HCO3 6, pO2 90. This patient is most likely suffering from which of the following? Review Topic The patient's presentation is consistent with diabetic ketoacidosis (DKA). DKA is a complication of diabetes mellitus type I, a deficiency of insulin (a hormone). DKA is a medical emergency that occurs in both type I and type II diabetics, although it Continue reading >>

Hyperosmolar Hyperglycemic State

Hyperosmolar Hyperglycemic State

Acute hyperglycemia, or high blood glucose, may be either the initial presentation of diabetes mellitus or a complication during the course of a known disease. Inadequate insulin replacement (e.g., noncompliance with treatment) or increased insulin demand (e.g., during times of acute illness, surgery, or stress) may lead to acute hyperglycemia. There are two distinct forms: diabetic ketoacidosis (DKA), typically seen in type 1 diabetes, and hyperosmolar hyperglycemic state (HHS), occurring primarily in type 2 diabetes. In type 1 diabetes, no insulin is available to suppress fat breakdown, and the ketones resulting from subsequent ketogenesis manifest as DKA. This is in contrast to type 2 diabetes, in which patients can still secrete small amounts of insulin to suppress DKA, instead resulting in a hyperglycemic state predominated simply by glucose. The clinical presentation of both DKA and HHS is one of polyuria, polydipsia, nausea and vomiting, volume depletion (e.g., dry oral mucosa, decreased skin turgor), and eventually mental status changes and coma. In patients with altered mental status, fingerstick glucose should always be checked in order to exclude serum glucose abnormalities. Several clinical findings pertaining only to DKA include a fruity odor to the breath, hyperventilation, and abdominal pain. HHS patients, in contrast to those with DKA, will present with more extreme volume depletion. The treatment of both DKA and HHS is primarily IV electrolyte and fluid replacement. Insulin for hyperglycemia may be given with caution and under vigilant monitoring of serum glucose. Other treatment options depend on the severity of symptoms and include bicarbonate and potassium replacement. Osmotic diuresis and hypovolemia Hypovolemia resulting from DKA can lead to acute Continue reading >>

Usmle Step 3- Endocrinology

Usmle Step 3- Endocrinology

DKA is more common in type 1 or type 2 DM? adipose tissue must have insulin to permit entry of glucose and FFAs; excess fat creates a deficiency of insulin if a pt cannot be well controlled with diabetes on metformin, what do you do? renal insufficiency (increases risk of lactic acidosis), pts using contrast agents for any radiologic or angiographic procedure (can lead to acute renal failure) increases release of insulin from pancreas sitagliptin, linagliptin, alogliptin, and saxagliptin, block metabolism or incretins such as glucagon-like peptide in Type 2 diabetes glucagon-like peptides; increase insulin release and decrease glucoagon secretion from the pancreas rosiglitazone and pioglitazone; increases peripheral insulin sensitivity acarbose, miglitol; block absorption of glucose at the intestinal lining alpha glucoside inhibitors like acarbose and miglitol have what side effects? diarrhea, abd pain bloating, and flatulence bc they block glucose absorption, sugar remains in the bowel available to bacteria and when bacteria eats the glucose they cast off gas and acid works like sulfonylureas (increases release of insulin from the pancreas); very short acting and can cause hypoglycemia SGLT inhibitor example to treat type 2 diabetes glargine aka lantus (use once a day), detemir, NPH (twice a day) increase insuin and decrease glucagon; examples are exenatide and liraglutide why do sulfonylureas do not work on type 1 diabetics? no functioning pancreas to stimulate to increase insulin release underproduction of insulin bc pancreas is destroyed hyperventilation, metabolic acidosis (low bicarb), fruity odor of the breath fro acetone and confusion from hyperosmolar state beta hydroxybutyrate/acetone level as a marker of ketone production; transcellular shift of potassium ou Continue reading >>

Diabetic Ketoacidosis Pathophysiology : Medicalschool

Diabetic Ketoacidosis Pathophysiology : Medicalschool

Please keep all topics germane to current medical students. ALL QUESTIONS GERMANE TO PREMEDICAL STUDENTS(for example how many doctors should I shadow to get into Harvard?) should be directed to the PREMED subreddit. Filesharing is prohibited in this subreddit. This includes discussion of filesharing or sources of pirated materials (e.g. anki decks). This subreddit is not a place to spam your blog or solicit business. Should you wish to submit your own content, please consider buying a sponsored link from reddit. Keep memes to a minimum. We welcome personal submissions and well-written concerns or stories, but please present them in a more intelligent fashion. Troll posts will not be tolerated. Previous examples of troll posts involved users seeking "help" on mundane or sensitive personal issues. These posts often include an immature or sophomoric subtext. As with memes, we ask you to please exercise judgement and present your content in a more mature and intelligent fashion. Moderator discretion is used to determine and remove posts of this nature. Please limit posts concerning USMLE Step 1 or 2 to their respective stickied threads. Posts not following this rule will be deleted. AMA-style threads are not allowed without prior moderator approval. Moderation issues related to the IRC channel should be directed at the mods of the respective channel. The moderators of the /r/MedicalSchool subreddit do not officially sanction/endorse any channel or take responsibility for any happenings within any channel. Posts made by accounts with less than 10 comment karma or less than 3 days old will be automatically removed. This is to prevent spam/trolling. For information on rules regarding recruitment for research studies, please see this page. You may not recruit for your research Continue reading >>

Hyperosmolar Hyperglycemic State (hhs)

Hyperosmolar Hyperglycemic State (hhs)

By Erika F. Brutsaert, MD, Assistant Professor, Albert Einstein College of Medicine; Attending Physician, Montefiore Medical Center Hyperosmolar hyperglycemic state is a metabolic complication of diabetes mellitus (DM) characterized by severe hyperglycemia, extreme dehydration, hyperosmolar plasma, and altered consciousness. It most often occurs in type 2 DM, often in the setting of physiologic stress. HHS is diagnosed by severe hyperglycemia and plasma hyperosmolality and absence of significant ketosis. Treatment is IV saline solution and insulin. Complications include coma, seizures, and death. Hyperosmolar hyperglycemic state (HHSpreviously referred to as hyperglycemic hyperosmolar nonketotic coma [HHNK] and nonketotic hyperosmolar syndrome) is a complication of type 2 diabetes mellitus and has an estimated mortality rate of up to20%, which is significantly higher than the mortality for diabetic ketoacidosis (currently < 1%). It usually develops after a period of symptomatic hyperglycemia in which fluid intake is inadequate to prevent extreme dehydration due to the hyperglycemia-induced osmotic diuresis. Acute infections and other medical conditions Drugs that impair glucose tolerance (glucocorticoids) or increase fluid loss (diuretics) Serum ketones are not present because the amounts of insulin present in most patients with type 2 DM are adequate to suppress ketogenesis. Because symptoms of acidosis are not present, most patients endure a significantly longer period of osmotic dehydration before presentation, and thus plasma glucose (> 600 mg/dL [> 33.3 mmol/L]) and osmolality (> 320 mOsm/L) are typically much higher than in diabetic ketoacidosis (DKA). The primary symptom of HHS is altered consciousness varying from confusion or disorientation to coma, usually as Continue reading >>

Pem Pearls: Treatment Of Pediatric Diabetic Ketoacidosis And The Two-bag Method

Pem Pearls: Treatment Of Pediatric Diabetic Ketoacidosis And The Two-bag Method

Insulin does MANY things in the body, but the role we care about in the Emergency Department is glucose regulation. Insulin allows cells to take up glucose from the blood stream, inhibits liver glucose production, increases glycogen storage, and increases lipid production. When insulin is not present, such as in patients with Type 1 diabetes mellitus (DM), all of the opposite effects occur. A lack of insulin causes the following downstream effects: Prevents glucose from being used as an energy source – Free fatty acids are used instead and produce ketoacids during metabolism. Causes a surge of stress hormones and induces gluconeogenesis – When blood glucose levels are elevated, the kidneys cannot absorb all of the glucose from the urine, and the extra glucose in the urine causes polyuria, even in the setting of dehydration. In addition, acidosis causes potassium to shift out of cells into the blood, and the combination of this with dehydration causes the body to preferentially retain sodium at the expense of potassium.1,2 When insulin homeostasis is disrupted and decompensates, patients are at risk for developing diabetic ketoacidosis (DKA). All of the following criteria are required for a diagnosis of DKA: Hyperglycemia (glucose >200 mg/dL) Acidosis (pH <7.3 or bicarb <15 mmol/L) Ketosis (by urine or blood test) Treatment is based on a simple principle: return the body’s glucose regulation to its normal state and replace all of the things the body consumed while insulin-deficient. While bolus insulin is common in the treatment of DKA in adults, it is relatively contraindicated in the pediatric patient. Dehydration and secondary sympathetic activation can interfere with local tissue perfusion and may cause irregular and unpredictable absorption. Step 1: Correction Continue reading >>

How To Order Bolus, Or Kcl On The Ccs Software - Step 3 - Uworld Forums For Usmle, Abim, Abfm, And Nclex Forums

How To Order Bolus, Or Kcl On The Ccs Software - Step 3 - Uworld Forums For Usmle, Abim, Abfm, And Nclex Forums

how to order BOLUS, or KCL on the ccs software i am practicing ccs . and nbme software, want to ask two qs 1. how to order iv bolus , e/g . patient in shock ... dka, etc. how to order the bolus, can't find it so far ... 2. how to order KCL infusion e.g dka patient needs potassium replacement , how to do that on the nbme software Did you search for normal saline bolus and normal saline with potassium infusion or whatever you base IV fluid is? I am not doing ccs currently but I was just wondering. BOLUS IS THE SAME AS IV FLUIDS , SOFTWARE OPTIMIZES EVERYTHING ITSELF , FOUND OUT JUST NOW POTASSIUM NEEDS TO ORDERED LIKE: KCL , IT WILL START IV KCL. About Us Contact Us Privacy Terms of Use Careers The United States Medical Licensing Examination (USMLE) is a joint program of the Federation of State Medical Boards (FSMB) and National Board of Medical Examiners (NBME). ABIM is registered trademark of American Board of Internal Medicine. ABFM is registered trademark of American Board of Family Medicine. NCLEX-RN and NCLEX-PN are registered trademarks of the National Council of State Boards of Nursing, Inc (NCSBN). MCAT is a registered trademark of the Association of American Medical Colleges (AAMC). SAT is a registered trademark of the CollegeBoard. ACT is a registered trademark of ACT, Inc. None of the trademark holders are affiliated with UWorld. Continue reading >>

Mnemonic Monday: Causes And Management Of Hyperkalemia: C Big K Di

Mnemonic Monday: Causes And Management Of Hyperkalemia: C Big K Di

Hyperkalemia is one of the most important and frequently encountered electrolyte abnormalities. Today’s post is intended to serve as a review of the most common causes of hyperkalemia and the approach to management of this electrolyte abnormality, both acutely and chronically. First, recall a few key concepts from normal potassium homeostasis: Potassium enters the body via oral intake or intravenous infusion Potassium is mainly stored within cells as the major intracellular cation; this is maintained by the Na-K-ATPase pump Potassium is excreted by the kidneys, and mineralocorticoids like aldosterone promote potassium excretion Hyperkalemia may thus result from any of the following causes: Excessive potassium intake (usually iatrogenic) Increased potassium release from cells (rhabdomyolysis, burns, hemolysis after blood transfusion, tumor lysis syndrome, extracellular shifts ? acidosis, insulin deficiency/DKA, beta blockers) Decreased potassium excretion (acute or chronic renal failure, potassium-sparing diuretics like spironolactone or amiloride, aldosterone deficiency, ACE inhibitors, angiotensin receptor blockers) Another common cause of an elevated serum potassium is “pseudohyperkalemia,” a laboratory artifact resulting from a hemolyzed blood sample. A repeat potassium level should be checked if psuedohyperkalemia is suspected. The most dangerous manifestations of hyperkalemia are cardiac conduction abnormalities and arrhythmias. Thus, the first step in the evaluation of hyperkalemia should be obtaining an EKG. Hyperkalemia may result in a progression of EKG changes including peaked T waves and QT interval shortening, PR and QRS interval prolongation, and finally a sine wave appearance. After obtaining an EKG, the approach to hyperkalemia management can be rem Continue reading >>

Effects Of Ph On Potassium: New Explanations For Old Observations

Effects Of Ph On Potassium: New Explanations For Old Observations

Go to: Abstract Maintenance of extracellular K+ concentration within a narrow range is vital for numerous cell functions, particularly electrical excitability of heart and muscle. Potassium homeostasis during intermittent ingestion of K+ involves rapid redistribution of K+ into the intracellular space to minimize increases in extracellular K+ concentration, and ultimate elimination of the K+ load by renal excretion. Recent years have seen great progress in identifying the transporters and channels involved in renal and extrarenal K+ homeostasis. Here we apply these advances in molecular physiology to understand how acid-base disturbances affect serum potassium. The effects of acid-base balance on serum potassium are well known.1 Maintenance of extracellular K+ concentration within a narrow range is vital for numerous cell functions, particularly electrical excitability of heart and muscle.2 However, maintenance of normal extracellular K+ (3.5 to 5 mEq/L) is under two potential threats. First, as illustrated in Figure 1, because some 98% of the total body content of K+ resides within cells, predominantly skeletal muscle, small acute shifts of intracellular K+ into or out of the extracellular space can cause severe, even lethal, derangements of extracellular K+ concentration. As described in Figure 1, many factors in addition to acid-base perturbations modulate internal K+ distribution including insulin, catecholamines, and hypertonicity.3,4 Rapid redistribution of K+ into the intracellular space is essential for minimizing increases in extracellular K+ concentration during acute K+ loads. Second, as also illustrated in Figure 1, in steady state the typical daily K+ ingestion of about 70 mEq/d would be sufficient to cause large changes in extracellular K+ were it not for Continue reading >>

Diabetic Ketoacidosis And Hyperglycaemic Hyperosmolar State

Diabetic Ketoacidosis And Hyperglycaemic Hyperosmolar State

The hallmark of diabetes is a raised plasma glucose resulting from an absolute or relative lack of insulin action. Untreated, this can lead to two distinct yet overlapping life-threatening emergencies. Near-complete lack of insulin will result in diabetic ketoacidosis, which is therefore more characteristic of type 1 diabetes, whereas partial insulin deficiency will suppress hepatic ketogenesis but not hepatic glucose output, resulting in hyperglycaemia and dehydration, and culminating in the hyperglycaemic hyperosmolar state. Hyperglycaemia is characteristic of diabetic ketoacidosis, particularly in the previously undiagnosed, but it is the acidosis and the associated electrolyte disorders that make this a life-threatening condition. Hyperglycaemia is the dominant feature of the hyperglycaemic hyperosmolar state, causing severe polyuria and fluid loss and leading to cellular dehydration. Progression from uncontrolled diabetes to a metabolic emergency may result from unrecognised diabetes, sometimes aggravated by glucose containing drinks, or metabolic stress due to infection or intercurrent illness and associated with increased levels of counter-regulatory hormones. Since diabetic ketoacidosis and the hyperglycaemic hyperosmolar state have a similar underlying pathophysiology the principles of treatment are similar (but not identical), and the conditions may be considered two extremes of a spectrum of disease, with individual patients often showing aspects of both. Pathogenesis of DKA and HHS Insulin is a powerful anabolic hormone which helps nutrients to enter the cells, where these nutrients can be used either as fuel or as building blocks for cell growth and expansion. The complementary action of insulin is to antagonise the breakdown of fuel stores. Thus, the relea Continue reading >>

More in diabetes