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Regulation of glucose in the body is done autonomically and constantly throughout each minute of the day. Normal BG levels should be between 60 and 140 mg/dL in order to supply cells of the body with its required energy. Brain cells don’t require insulin to drive glucose into neurons; however, there must still be normal amounts available. Too little glucose, called hypoglycemia, starves cells, and too much glucose (hyperglycemia) creates a sticky, paralyzing effect on cells. Euglycemia, or blood sugar within the normal range, is naturally ideal for the body’s functions. A delicate balance between hormones of the pancreas, intestines, brain, and even adrenals is required to maintain normal BG levels.

Hormones of the Pancreas
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Regulation of blood glucose is largely done through the endocrine hormones of the pancreas, a beautiful balance of hormones achieved through a negative feedback loop. The main hormones of the pancreas that affect blood glucose include insulin, glucagon, somatostatin, and amylin.

Insulin (formed in pancreatic beta cells) lowers BG levels, whereas glucagon (from pancreatic alpha cells) elevates BG levels.

Somatostatin is formed in the delta cells of the pancreas and acts as the “pancreatic policeman,” balancing insulin and glucagon. It helps the pancreas alternate in turning on or turning off each opposing hormone.

Amylin is a hormone, made in a 1:100 ratio with insulin, that helps increase satiety, or satisfaction and state of fullness from a meal, to prevent overeating. It also helps slow the stomach contents from emptying too quickly, to avoid a quick spike in BG levels.

As a meal containing carbohydrates is eaten and digested, BG levels rise, and the pancreas turns on insulin production and turns off glucagon production. Glucose from the bloodstream enters liver cells, stimulating the action of several enzymes that convert the glucose to chains of glycogen—so long as both insulin and glucose remain plentiful. In this postprandial or “fed” state, the liver takes in more glucose from the blood than it releases. After a meal has been digested and BG levels begin to fall, insulin secretion drops and glycogen synthesis stops. When it is needed for energy, the liver breaks down glycogen and converts it to glucose for easy transport through the bloodstream to the cells of the body (Wikipedia, 2012a).

In a healthy liver, up to 10% of its total volume is used for glycogen stores. Skeletal muscle cells store about 1% of glycogen. The liver converts glycogen back to glucose when it is needed for energy and regulates the amount of glucose circulating between meals. Your liver is amazing in that it knows how much to store and keep, or break down and release, to maintain ideal plasma glucose levels. Imitation of this process is the goal of insulin therapy when glucose levels are managed externally. Basal–bolus dosing is used as clinicians attempt to replicate this normal cycle.

While a healthy body requires a minimum concentration of circulating glucose (60–100 mg/dl), high chronic concentrations cause health problems and are toxic:

Acutely: Hyperglycemia of greater than 300 mg/dl causes polyuria, resulting in dehydration. Profound hyperglycemia ( greater than 500 mg/dl) leads to confusion, cerebral edema, coma, and, eventually, death (Ferrante, 2007).
Chronically: Hyperglycemia that averages more than 120 to 130 mg/dl gradually damages tissues throughout the body and makes a person more susceptible to infections. The glucose becomes syrupy in the bloodstream, intoxicating cells and competing with life-giving oxygen.
The concentration of glucose in the blood is determined by the balance between the rate of glucose entering and the rate of glucose leaving the circulation. These signals are delivered throughout the body by two pancreatic hormones, insulin and glucagon (Maitra, 2009). Optimal health requires that:

When blood glucose concentrations are low, the liver is signaled to add glucose to the circulation.
When blood glucose concentrations are high, the liver and the skeletal muscles are signaled to remove glucose from the circulation.

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DKD, or diabetic nephropathy: pathophysiology, symptoms, risk factors, diagnosis and management. For patient education. This video is available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/narrated-videos-by-topics/diabetes/-/medias/0079bcc6-2a8f-48d6-947d-57b464d2e271-diabetic-kidney-disease-narrated-animation
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Diabetic kidney disease, or diabetic nephropathy, is kidney disease caused by diabetes. It’s a very common diabetic complication, affecting about one third of people with diabetes type 1, and half of those with diabetes type 2. Diabetic kidney disease is responsible for most of the excess mortality associated with diabetes.
Because the kidneys remove metabolic wastes, control blood pH, regulate fluid and electrolyte balance, as well as produce several hormones; loss of kidney function results in accumulation of toxic wastes, electrolyte imbalances, and a number of other health problems.
The disease develops slowly over time, progressing from renal insufficiency to end-stage renal failure. Often, initial loss of renal tissue does not produce any symptoms. Symptoms typically appear when a significant portion of kidney function is already lost. The ability to concentrate urine is usually the first to be impaired, resulting in frequent trips to the bathroom, especially at night. Other early signs include fatigue, loss of appetite, and decreased mental ability.
Chronic high blood glucose levels, together with high blood pressure caused by diabetes, bring damage to tiny blood vessels in the kidneys, affecting their functions. Cellular degeneration in the functional units of the kidneys, the nephrons, in particular the podocytes of renal glomeruli, further contributes to the impairment of renal functions.
Diabetes, especially when poorly managed, is the biggest risk factor for chronic kidney disease. Other risk factors are the same as those for high blood pressure and include smoking, having high cholesterol levels, and being overweight.
Because initial loss of renal tissue does not produce any symptoms, it is important for diabetic patients to test annually for kidney functions. The tests typically include blood and urine analysis.
Prevention and management strategies consist of controlling blood sugar levels, blood pressure, and cholesterol levels; all of which can be achieved with a combination of lifestyle changes and medications.
Lifestyle measures typically include a healthy diet with low salt intake, increased physical activity, weight management, and smoking cessation.
Among all blood pressure lowering medications, ACE inhibitors and angiotensin receptor blockers, which block the renin–angiotensin–aldosterone system, work best to protect kidney functions.
End-stage kidney disease requires dialysis or kidney transplantation.
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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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Damage to the nervous system is the most common complication of diabetes mellitus. Types of diabetic neuropathy: peripheral neuropathy, autonomic neuropathy, mononeuropathy and proximal neuropathy. Pathophysiology, symptoms, complications and treatments. For patient education. This video is available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/narrated-videos-by-topics/diabetes/-/medias/3eea39ab-f6be-4dbd-b7ef-131d90d59b3a-diabetic-neuropathy-narrated-animation
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Diabetic neuropathy is nerve damage caused by diabetes. It is the most common diabetic complication, affecting at least 50% of all patients.
Chronic high blood sugar levels cause progressive injury to neurons. Sensory neurons are usually the first to be affected, followed by autonomic neurons that control internal organs. Rarely, motor neurons that activate voluntary movements may also be impaired later in the disease, albeit to a lesser extent.
There are several types of diabetic neuropathy. A patient may develop more than one type at a time.
The most common is peripheral neuropathy. It’s also called “distal symmetric polyneuropathy” because it typically involves multiple peripheral nerves, on both sides of the body, and affects the longest sensory axons that convey sensations from the feet, legs, and hands. Symptoms develop on the body in that order and include numbness, tingling, or burning sensation, which usually worsen at night. Sensitivity to pain can either be exaggerated, or, on the contrary, lost. Loss of sensation leads to increased risk of painless injuries, which often go unnoticed and therefore untreated. This, together with slow healing caused by diabetes, can turn minor cuts or blisters into serious infections.
Autonomic neuropathy affects nerves that control activities of internal organs.
In cardiac autonomic neuropathy, nerves that regulate heart rate and blood pressure are damaged. As a result, the body reacts more slowly to change of position, and patients may feel lightheadedness when standing up. Other signs include rapid heart rates, or sudden, unexplained changes in heart rate.
In the digestive system, nerve damage may cause nausea, vomiting, loss of appetite, difficulty swallowing, slow stomach emptying, and bowel problems.
Neuropathy in the urinary and reproductive systems may lead to urinary retention, hesitancy, urinary incontinence, and sexual dysfunctions.
Nerve damage in the eyes can cause slower adjustment to changes in light and darkness.
Nerve damage in sweat glands may result in either absence of sweat or heavy sweating, especially at night; different parts of the body may also produce sweat differently.
Another effect of autonomic neuropathy is hypoglycemia unawareness, meaning the body is unaware when blood sugar levels are low. Warning signs such as hunger or dizziness cannot be felt, and patients may pass out before taking steps to increase their blood sugar.
Mononeuropathy, or focal neuropathy, is dysfunction of a single nerve, typically due to entrapment. A common example is carpal tunnel syndrome, in which the median nerve is compressed as it passes through a narrow tunnel in the wrist, causing pain, numbness, and tingling in the hand. Damage to a cranial nerve can cause problems with vision or loss of control of facial muscles.
Proximal neuropathy is a rare type of nerve damage affecting the thighs, hip, buttock, and occasionally, the abdomen or chest, typically on one side of the body. Symptoms include severe pain in the affected areas, and thigh muscle weakness and wasting.
Diabetic neuropathy can be prevented by effectively controlling blood sugar levels. Managing diabetes also helps slow the progression of damage.
Treatments aim to relieve pain and symptoms, to restore functions and prevent further complications. Treatments vary depending on the affected organs.

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(USMLE topics) Mechanisms by which obesity and physical inactivity can cause pre-diabetes and diabetes. This video is available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/narrated-videos-by-topics/diabetes/-/medias/b42e945a-389f-41d0-b592-77aad378a24d-how-unhealthy-lifestyle-causes-prediabetes-and-diabetes-narrat
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Diabetes refers to a group of conditions characterized by high levels of blood glucose, commonly known as blood sugar. Glucose comes from digestion of carbohydrates in food, and is carried by the bloodstream to various body tissues. But glucose cannot cross the cell membrane to enter the cells on its own; to do so, it requires assistance from a hormone produced by the pancreas called insulin. Binding of insulin to its receptor on a target cell triggers a signaling cascade that brings glucose transporters to the cell membrane, creating passageways for glucose to enter the cells. In most tissues, muscles for example, glucose is used as an energy source, while in the liver and adipose tissue, it is also stored for later use, in the form of glycogen and fats. When the body is in the fasted state, the liver produces and secretes glucose into the blood, while adipose tissues release free fatty acids to the liver where they are converted into additional metabolic fuel.
Diabetes happens when insulin is either deficient or its action is compromised. Without insulin, glucose cannot enter the cells; it stays in the blood, causing high blood sugar levels.
There are 2 major types of diabetes. Type 1 is when the pancreas does not produce enough insulin; and type 2 is when the body’s cells do not respond well to insulin – they are insulin-resistant. Both types are caused by a combination of genetic and environmental factors but genetics plays a major role in type 1, while lifestyle is a predominant risk factor for type 2. For this reason, type 1 diabetes usually starts suddenly in childhood, while type 2 progresses gradually during adulthood, going through a so called pre-diabetic stage, which is defined as borderline blood sugar levels. Pre-diabetes is very common. Unhealthy lifestyle is the trigger of pre-diabetes and the main driving force behind its progression to diabetes type 2. The key factors are obesity and physical inactivity.
There are at least 2 ways by which obesity can cause insulin resistance and high blood glucose.
First, in obesity, fat cells have to process more nutrients than they can manage and become stressed. As a result, they release inflammatory mediators, known as cytokines. Cytokines interfere with the signaling cascade by insulin receptor, blocking the action of insulin.
Second, excess adipose tissue releases abnormally large amount of free fatty acids to the liver – an event that normally happens only when the body is fasting. This tricks the liver into producing and releasing more glucose into the blood. High blood glucose stimulates further insulin secretion. Constant high insulin levels de-sensitize body tissues, causing insulin insensitivity.
Intra-abdominal fat appears to produce more fatty acids and cytokines, and therefore has more severe effect on blood glucose, than subcutaneous, or peripheral fat. For this reason, large waist size is a greater risk factor than high body mass index.
Sedentary lifestyle, apart from having indirect effect by causing weight gain, has its own direct impact on insulin resistance. This is because physical activity is required to maintain healthy blood sugar levels. Physical activity increases energy demand by the muscles, which consume glucose from the blood, and subsequently from glucose storage in the liver and adipose tissue. High energy expenditure helps to clear up faster the spikes of blood glucose that follow every meal. High energy demand also promotes better cellular response to insulin, increasing insulin sensitivity. Physical inactivity, even for a short period of time, results in consistently higher spikes of blood sugar after meals, which can trigger pre-diabetic changes in healthy individuals, or speed up transition from pre-diabetes to diabetes. This happens not only to over-weight patients, but also to people with seemingly healthy weight.
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Definition, diagnosis, risk factors, treatments. This video is available for instant download licensing here: https://www.alilamedicalmedia.com/-/galleries/images-videos-by-medical-specialties/metabolism/-/medias/ecf4765f-4f5d-41f0-ae11-54d1827ebf82-metabolic-syndrome-narrated-animation
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Metabolic syndrome, also called syndrome X or insulin resistance syndrome, refers to a combination of metabolic risk factors that increase the chance of developing cardiovascular diseases, such as heart attacks or strokes; and type 2 diabetes.
Metabolic syndrome is diagnosed when a patient has at least three of the following:
– A waistline of 40 inches or more for men, or 35 inches or more for women;
– A systolic blood pressure above 130 and a diastolic blood pressure above 85 mmHg, or if the patient is taking blood pressure-lowering medications;
– A fasting blood sugar level above 100 mg/dL, or if the patient is taking glucose-lowering medications;
– A triglyceride level greater than 150 mg/dL;
– An HDL level of less than 40 mg/dL for men, or 50 mg/dLfor women.
Metabolic syndrome, in turn, has its own set of underlying risk factors, of which insulin resistance is most important. Insulin resistance is when the body’s cells do not respond well to insulin and therefore cannot use glucose; glucose stays in the blood, causing high blood sugar levels while the cells are deprived of nutrition. Insulin resistance can be acquired, hereditary, or mixed. Other risk factors include abdominal obesity, physical inactivity, aging, hormonal imbalances, and use of certain medications. Women are more susceptible than men. Some racial and ethnic groups are at higher risk than others.
Metabolic syndrome is often associated with excessive blood clotting and chronic low-grade inflammation, as well as several other conditions, but the cause-effect relationship is not clear.
The goal of treating metabolic syndrome is to reduce the risk of cardiovascular diseases. Treatment aims to lower blood pressure and cholesterol; and to manage diabetes, or prevent it, if it hasn’t already developed.
Lifestyle changes include a heart-healthy diet, physical activity plan, weight management, stress management, and quitting smoking.
If lifestyle changes aren’t enough, medications may be prescribed to lower LDL cholesterol and triglycerides; to reduce blood pressure, blood sugar level, or to prevent blood clots.
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Diabetes mellitus is a group of metabolic diseases that causes a person to have high blood sugar, either because the body does not produce enough insulin, or because cells do not respond to the insulin that is produced. It’s also a disease of the immune system.

Diabetes affects about 8 percent of the U.S. population or 25 million people. 285 million worldwide. It is estimated that half of all Americans will have diabetes by 2020.

High blood sugar produces the classical signs and symptoms of diabetes: thirst, hunger, weight loss, frequent urination…
Type 2 diabetes is a consequence of a seismic shift in lifestyle beginning about ten thousand years ago.

The shift was from hunting and gathering food to farming and raising animals, then eating the fruit of that labor. Before the shift, Neolithic hunter gatherers gorged food to store body fat in good times to ward off starvation in lean times. Body fat was life insurance!

Today, gobbling food in excess has developed into a pathology linked to obesity, type 2 diabetes, heart disease, and stroke. .
Type 1 Diabetes results from autoimmune destruction of insulin producing beta cells of the pancreas. Incidence varies from eight to 17 per 100 thousand in the U.S. It is fatal unless treated with insulin.
.
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(USMLE topics) This is an updated version to include explanation of symptoms and complications. This video is available for instant download licensing here https://www.alilamedicalmedia.com/-/galleries/narrated-videos-by-topics/diabetes/-/medias/b13f42e3-24ec-4b99-85b8-1decf0535101-updated-diabetes-narrated-animation-full-version
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Diabetes mellitus refers to a group of conditions characterized by high levels of blood glucose, commonly referred to as blood sugar.
During digestion, carbohydrates in food are broken down into glucose which is carried by the bloodstream to various organs of the body. Glucose is taken up by the cells and is either consumed as an energy source or stored for later use. Insulin is a hormone produced by beta cells of the pancreas and is necessary for driving glucose into cells. Binding of insulin to its receptor on target cells triggers a signaling cascade that brings glucose transporters to the cell membrane. When insulin is deficient, glucose cannot enter the cells; it stays in the blood, causing high blood sugar levels while the cells are deprived of nutrition. This results in unexplained weight loss and increased hunger. As blood sugar level exceeds the ability of the kidneys to reabsorb, it overflows into urine, taking water along with it, resulting in large volumes of urine, dehydration and excessive thirst.
In the long run, too much sugar in the blood may cause damages to blood vessels, resulting in increased risks of cardiovascular diseases such as heart attack and stroke. Damaged vessels in the eyes may lead to loss of vision; while in the kidneys, renal failure may result. High blood sugar is also toxic to the nerves, resulting in numbness, tingling and reduced pain perception. This, together with impaired wound healing can lead to development of skin ulcers, most commonly in the feet.
Acute hyperglycemic crises may develop when diabetic patients undergo additional stress such as infections, other illness or inadequate treatment. These complications involve severe disturbances of blood homeostasis and are potentially life-threatening.
There are two major types of diabetes mellitus.
In type 1, beta cells of the pancreas are destroyed by the body’s own immune system by mistake. The exact mechanism remains unclear, but genetic factors are believed to play a major role, with at least 50 genes involved in predisposition to the disease. Insulin production is reduced; less insulin binds to its receptor on target cells; less glucose is taken into the cells; more glucose stays in the blood. Type 1 is characterized by early onset, symptoms usually start suddenly, before the age of 20. Type 1 diabetes is “insulin dependent” and can be successfully managed with insulin replacement.
In type 2 diabetes, the pancreas produces enough insulin but something goes wrong either with receptor binding or the signaling cascade in the target cells. The cells are not responsive to insulin and therefore cannot import glucose. Type 2 diabetics are said to be “insulin resistant”. Here again, genetic factors predispose susceptibility to the disease, but lifestyle plays a major role. Type 2 is characterized by adult onset; symptoms appear gradually, usually after the age of 30. Management focuses on weight loss and includes a low-carb diet.
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Diabetes mellitus (DM) occurs when the body either produces insufficient amounts of insulin (type 1 diabetes), or the body build resistance to insulin due to overuse (type 2 diabetes). In this NCLEX review, Mike Linares RN reviews insulin types, memory tricks on how to remember insulin peak times, onset, and duration of:
Rapid acting insulin: Lispro, Aspart, Glulisine (brand names: Humalog, Novolog, Apidra)
Short acting insulin: Regular Insulin (Humulin, Acrapid, Novolin)
Intermediate acting insulin: NPH, Lente
Long acting insulin: Glargine insulin, Detemir insulin (brand names: Lantus, Levemir)

The pathophysiology of type 1 diabetes is where the pancreas does not produce insulin, and type two diabetes is where the body develops insulin resistance.

Pharmacology of type one diabetes includes insulin subcutaneous injection and insulin pump, and type two diabetes mellitus includes adherance to diet, oral antidiabetics as well as insulin.

Both could be exacerbated into extreme conditions, DKA (diabetes ketoacidosis) more common in type one diabetes, and HHS or HHNS (hyperglycemic hyperosmolar syndrome).

This 7 part video series on endocrine medical surgical adult health nursing is intended to help registered nurse RN students and LPN students with NCLEX memorization tricks. In this video series Michael Linares, RN from Simple Nursing helps explain the nursing pathophysiology, signs and symptoms, causes, pathology, treatment options for various diagnosis, which are expected to know for the NCLEX, HESI, ATI, and Kaplan proctor exams.

For more information on NCLEX endocrine medical surgical nursing topics like Cushings and Addison nursing treatments, diabetes mellitus and insulin onset, peak and duration memory tricks for NCLEX RN and LPN, click here: https://simplenursing.com/free-trial/

Frustrated with boring NCLEX programs “included” in your tuition? Check out the SimpleNursing NCLEX prep mobile app: https://simplenursing.com/free-trial/
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Need help with other difficult nursing school topics?
Click below. We got you covered 🙂
– Fluid & Electrolytes https://www.youtube.com/playlist?list=PL3NAm8UHLUnLJSqeCM_EJHXZ685sb67bn
– Heart Failure (CHF) https://www.youtube.com/playlist?list=PL3NAm8UHLUnLEVzZvkdBX1IWHPg21Jobw
– Myocardial Infarction (MI) https://www.youtube.com/playlist?list=PL3NAm8UHLUnLLJQsAIsQaHJiOvcLN1cUe
– Addison’s vs. Cushing https://www.youtube.com/playlist?list=PL3NAm8UHLUnKT3JBkVTN-hXbyULbPgWz5
– Diabetes Mellitus & DKA vs HHNS https://www.youtube.com/playlist?list=PL3NAm8UHLUnKxNrh1HdilzIIH9WM8JrLq
– Cardiomyopathy https://www.youtube.com/playlist?list=PL3NAm8UHLUnIeh0g_moaGLzXWiOh3fqdi
– IV Fluids: Hypertonic, Hypotonic & Isotonic https://www.youtube.com/playlist?list=PL3NAm8UHLUnIdjUfgMcAE1JIq6Nx29JRX
– Hypertension https://www.youtube.com/watch?v=5zg95R8H1oo
– Hyperkalemia https://youtu.be/HdG8lqJzWi4
– SIADH vs Diabetes Insipidus https://youtu.be/hKFGGv0E-5A

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