Patho Chapter 33: Diabetes mellitus & metabolic syndrome

Retinopathies

-Diabetes is the leading cause of acquired blindness in the US -Causes vascular permeability in retina, microaneursyms, hemorrhage, neovascularization, scarring, retinal detachment

The patient is prescribed 30 units of regular insulin and 70 units of insulin isophane suspension (NPH insulin) subcutaneously every morning. The nurse should provide which instruction to the patient for insulin administration?

"Draw up the regular insulin into the syringe first, followed by the cloudy NPH insulin."

When teaching a patient about insulin glargine (Lantus), which statement by the nurse about this drug is correct?

"You cannot mix this insulin with regular insulin and thus will have to take two injections."

what happens to glucose after you eat

-glucose levels rise & insulin is released from the beta cells in the pancreas & beginning to transport glucose to into the cell -glucose removed from blood & stored in liver as glycogen

Insulin

-only hormone that lowers blood glucose levels 1. promotes glycogen formation from glucose in liver 2.prevents fat & glycogen breakdown (glycogenolysis) 3.inhibits gluconeogenesis & increases protein synthesis and promotes fat storage

Explain the causes of DKA.

1. Are uncontrolled diabetes because if blood glucose is not mointored closely, the sugar level in the blood will increase. 2. Insufficient insulin doe or unknown new-onset type I diabetes because not enough insulin medication is taken to bring blood glucose down to normal range. 3. Skipping insulin doses which causes blood glucose levels to become elevated. 4. Stress which increases blood glucose normally, but those with diabetes need to monitor the glucose more closely during times of stress and adjust insulin accordingly.

Explain the symptoms of DKA.

1. Decreased LOC due to metabolic acidosis and shock. 2. Severe hypovolemia due to shock. 3. Electrolyte imbalances, especially potassium problems. 4. Polyuria initially to excrete excess sugar which causes hypovolemia. 5. Polyuria can progress into oliguria if the kidneys are not adequately perfused.

Explain the manifestations of HNNK.

1. Dehydration 2. Hyperosmolar plasma 3. Weakness, polyuria, excessive thirst, hemiparesis, aphasia, Babinski reflex, hyperthermia, visual hallucinations, seizures. 4. May be mistaken for a stroke initially.

Hypoglycemia symptoms

1. Sweating, increased pulse, nervousness, irritability, and tremors because of stimulation of the SNS and release of epinephrine. 2. Dizziness, headache, slurred speech, decreased coordination, and confusion may also occur if the CNS becomes depressed due to lack of glucose.

Explain the causes of hypoglycemia.

1. Too much insulin through oral or injected anti-diabetic agents because they decrease blood sugar. 2. Decreased food intake because it decreases blood sugar and is worse if the patient is also on anti-hyperglycemic medications. 3. Increased activity because it increases cellular metabolism.

Explain the diagnosis of DKA.

1. Urinalysis will show glycosuria and ketonuria. 2. Blood gases will show a low pH indicating acidosis. 3. Hyperkalemia may be present. 4. BUN and creatinine should also be checked to verify kidney function.

the pancreas is made up of 2 major tissues

1. acini 2. islets of langerhans

3 major acute complications of impaired blood glucose regulation

1. diabetic ketoacidosis(DKA), 2. HHS(hypergylcemic hyperosmolar state, and 3.) hypoglycemia-- all of these are life threatening conditions

metabolic syndrome

1. insulin resistance 2. increased glucose production by the liver 3. impaired secretion of insulin by pancreatic beta cells must have 3 or more of the following: abdominal obesity, elevated triglycerides, elevated BP/hypertension, decreased HDL, elevated fasting blood glucose, macrovascular disease (CAD, PAD)

Metabolic Abnormalities of Type 2 Diabetes

1. insulin resistance 2. increase glucose production by the liver 3. impaired secretion of insulin by the pancreatic beta cells

weight loss is associated with which type of diabetes?

type 1 DM

The nurse is providing education to a patient for the prescription glipizide (Glucotrol). The nurse explains this medication is more effective when administered at which time?

30 minutes before a meal

s/s of type 1

3p's (polyuria, polydipsia, polyphagia), weight loss

Assuming the patient eats breakfast at 8:30 AM, lunch at noon, and dinner at 6:00 PM, he or she is at highest risk of hypoglycemia after an 8:00 AM dose of NPH insulin at what time?

5:00 PM

Diabetes Diagnostic Tests

8 hr FBS>126 Random BG>200 OGTT>200 or more in the 2 hr sample

Describe the etiology, pathophysiology, clinical manifestations, and the specific role metabolic syndrome plays in the development of Type II diabetes mellitus: role of adipose tissue in the development of type II diabetes mellitus.

Although many details of the relationship between adipose tissue, insulin resistance, and increased glucose production in obese people with type 2 diabetes remain to be elucidated, several pathways have been proposed. Primary among these is the role of an increased concentration of free fatty acids (FFAs). Visceral obesity is accompanied by an increase in postprandial FFA concentrations and subsequent triglyceride storage, including in sites that do not normally store fat such as the liver, skeletal muscle, heart, and pancreatic beta cells. This has several consequences. First, excessive and chronic elevation of FFAs can directly cause pancreatic beta cell dysfunction (lipotoxicity). Second, at the level of the peripheral tissues, FFAs inhibit glucose uptake and glycogen storage. Third, the accumulation of FFAs and triglycerides reduces hepatic insulin sensitivity, leading to increased hepatic glucose production and hyperglycemia, especially in the fasting state. In the liver, the uptake of FFAs from the portal blood can lead to hepatic triglyceride accumulation and nonalcoholic fatty liver disease. In addition to the metabolic effects of visceral obesity, adipocytes are the source of a number of important factors (e.g., adiponectin, leptin, FFAs) involved in a wide range of other processes, including glucose and lipid metabolism, inflammation, and thrombosis. In obesity and type 2 diabetes, there is a reduction in the production of some factors that are normally synthesized by adipocytes (i.e., adiponectin), whereas there is an accelerated release of other factors such as angiotensinogen, plasminogen activator inhibitor-1, leptin, and proinflammatory cytokines (e.g., tumor necrosis factor-α). Adiponectin, which is secreted by adipocytes and circulates in the blood, is the only known adipocyte-secreted factor that increases tissue sensitivity to insulin. It has been shown that decreased levels of adiponectin coincide with insulin resistance in persons with obesity and type 2 diabetes. In skeletal muscle, adiponectin has been shown to decrease tissue triglyceride content by increasing the use of fatty acids as a fuel source. Adiponectin also appears to have antidiabetes, anti-inflammatory, and antiatherogenic effects.

Hypoglycemia S/S

BG<60 mg/dl Rapid onset of ANS repsonses: Hunger, lightheadedness, shakiness H/a Anxiety, irritability Pale, cool, skin Diaphoresis Irritable Normal/shallow respirations Tachycardia/palpitations Gradual onset of Impaired Cerebral Function Strange or unusual feelings Decreased LOC Difficulty in thinking and inability to concentrate Change in emotional behavaior Slurred speech h/a, blurred vision Seizures leading to comas Hunger Lightheadedness Headache Tachycardia

Hyperglycemia

BG>250 Thirst Polyuria (early) oliguria( late) N/V, abd pain Skin that is warm, dry, flushed with poor skin turgor Dry mucous membranes Confusion Weakness Lethargy Weak pulse Diminished reflexes Rapid, deep respirations with acetone/fruity odor due to Ketones (Kussmal Respirations)

Metformin (Glucophage) drug class

Biguanide

Hyperglycemia S/S

Blurred vision Fatigue Parathesias Skin infection

Explain chronic DM complications

Chronic complications of diabetes mellitus result from micro and macrovascular damages. Macrovascular complications are CAD, PVD, and cerebrovascular disease because of related issue like hypertension, sedentary lifestyle, lipid abnormalities, smoking and hyperglycemia. Microvascular complications include nephropathy (kidney damage), neuropathy (burning of the feet or ED), retinopathy (damage to the retina) due to hyperglycemia damaging the nerves and blood vessels. Neuropathies are nerve dysfunctions related to progressive deterioration of nerves leading to decreased nerve function. Damage to sensory nerve fibers leads to pain and loss of sensation. Paresthesia refers to the burning, prickling, or stinging sensation in the extremities and it is caused by glucose damage to nerves. The blood vessels thicken and narrow which decrease blood flow to the area and results in ischemia or necrosis. Smaller blood vessels lead or are destroyed and that decreases the delivery of nutrients and oxygen to tissues.

Which oral hypoglycemic drug has a quick onset and short duration of action, enabling the patient to take the medication 30 minutes before eating and skip the dose if he or she does not eat?

Repaglinide (Prandin)

acute complications of diabetes

DKA (Diabetic KetoAcidosis) , hyperosmolar hyperglycemic state, hypoglycemia

ph

Diabetes can make the levels to become more acidic and develop a condition called ketoacidosis. Causing the levels to decrease.

Describe the etiologies, pathophysiology, and acute complications of diabetic ketoacidosis (DKA).

Diabetic ketoacidosis is a serious complication of diabetes that occurs when your body produces high levels of blood acids called ketones. The condition develops when your body can't produce enough insulin. Insulin normally plays a key role in helping sugar (glucose) enter your cells. Without enough insulin, your body begins to break down fat as fuel. This process produces a buildup of acids in the bloodstream called ketones, eventually leading to diabetic ketoacidosis if untreated. The development of DKA is commonly preceded by a day or more of polyuria, polydipsia, nausea, vomiting, and marked fatigue, with eventual stupor that can progress to coma. Abdominal pain and tenderness may be experienced without abdominal disease. The breath has a characteristic fruity smell because of the presence of volatile ketoacids. Hypotension and tachycardia may be present because of a decrease in blood volume. A number of the signs and symptoms that occur in DKA are related to compensatory mechanisms. The heart rate increases as the body compensates for a decrease in blood volume, and the rate and depth of respiration increase (i.e., Kussmaul respiration) as the body attempts to prevent further decreases in pH. [A DIABETIC COMPLICATION WHERE TO BODY PRODUCES EXCESS BLOOD ACIDS (KETONES).]

Explain DKA

Diabetic ketoacidosis is when there is lack of insulin and glucose can not enter cells. The cells are starved and the body breaks down fat for energy. Fat breakdown results in ketones which are an acid. Ketones in the blood cause metabolic acidosis which causes DKA.

Dawn phenomenon

Early morning glucose elevation produced by the release of growth hormone, which decreases peripheral uptake of glucose resulting in elevated morning glucose levels. Admin of insulin at a later time in day will coordinate insulin peak with the hormone release.

Glycosylated hemoglobin (HbA1c)

Expected range: 4%-6% Target for diabetics: 6.5%-8% Total target goal<7%

Explain HNNK.

HHNK is characterized by hyperglycemia, hyper-osmolarity, and dehydration in the absence of acidosis. This complication presents similarly to DKA but without acidosis. The body makes enough insulin to prevent breakdown of fat so there is no ketone formation.

Based on the pathophysiology of diabetes mellitus explain why foot ulcers and infection are so common and can lead to extremely devastating effects in patients.

Foot problems are common among people with diabetes and may become severe enough to cause ulceration, infection, and, eventually, the need for amputation. Foot problems have been reported as the most common complication leading to hospitalization among people with diabetes. They represent the effects of neuropathy and vascular insufficiency. Distal symmetric neuropathy is a major risk factor for foot ulcers. People with sensory neuropathies have impaired pain sensation and often are unaware of the constant trauma to the feet caused by poorly fitting shoes, improper weight bearing, hard objects or pebbles in the shoes, or infections such as athlete's foot. Neuropathy may prevent people from detecting pain; they are unable to adjust their gait to avoid walking on an area of the foot where pressure is causing trauma and necrosis. Motor neuropathy with weakness of the intrinsic muscles of the foot may result in foot deformities, which lead to focal areas of high pressure. When the abnormal focus of pressure is coupled with loss of sensation, a foot ulcer can occur. Common sites of trauma are the back of the heel, the plantar metatarsal area, or the great toe, where weight is borne during walking.

Risk Factors for DM

Genetics can predispose a person to occurrence of type 1 and type 2 toxins and viruses can predispose an individual to deiabetes by destroying beta cells, leading to type 1 obesity, physical inactivity, high triglycerides (greater than 250) HTT may lead to insulin resistance and type II

When caring for a pregnant patient with gestational diabetes, the nurse should question a prescription for which drug?

Glipizide (Glucotrol)

The nurse will instruct the patient to treat hypoglycemia with which drug?

Glucagon (GlucaGen)

hyperosmolar

Glucose greater than 600 mg, Type 2 diabetics have this. . Signs: dehydration, weakness, diabetic coma if not treated, polyuria, polydipsia

nephropathies

Having diabetes for a long time. Capillaries in nephron form lesions.Decrease in filtration in the kidneys causing kidney failure. Lose plasma proteins in urine and decrease blood colloid osmotic pressure

Describe the etiologies, pathophysiology, and acute complications of hypoglycemia.

Hypoglycemia, or an insulin reaction, occurs from a relative excess of insulin in the blood and is characterized by below-normal blood glucose levels. It occurs most commonly in people treated with insulin injections, but prolonged hypoglycemia also can result from some oral hypoglycemic agents (i.e., sulfonylurea). There are many factors that can precipitate an insulin reaction in a person with type 1 or type 2 diabetes, including error in insulin dose, failure to eat, increased exercise, decreased insulin need after removal of a stress situation, medication changes, and a change in insulin injection site. Hypoglycemia usually has a rapid onset and progression of symptoms. The signs and symptoms of hypoglycemia can be divided into two categories: (1) those caused by altered cerebral function and (2) those related to activation of the autonomic nervous system. Because the brain relies on blood glucose as its main energy source, hypoglycemia produces behaviors related to altered cerebral function. Headache, difficulty in problem solving, disturbed or altered behavior, coma, and seizures may occur. At the onset of the hypoglycemic episode, activation of the parasympathetic nervous system often causes hunger. The initial parasympathetic response is followed by activation of the sympathetic nervous system; which causes anxiety, tachycardia, sweating, and a cool and clammy skin due to constriction of the skin vessels. The signs and symptoms of hypoglycemia are highly variable, especially in children and the elderly, and not everyone manifests all or even most of the symptoms. Elderly people may not display the typical autonomic responses, but typically do display signs of altered cerebral function, including mental confusion. Also, some medications, such as β-adrenergic blocking drugs, interfere with the autonomic response normally seen in hypoglycemia. Some people develop hypoglycemic unawareness.

Which is a rapid-acting insulin with an onset of action of less than 15 minutes?

Insulin aspart (NovoLog)

Which long-acting insulin mimics natural, basal insulin with no peak action and a duration of 24 hours?

Insulin glargine (Lantus)

Long acting

Insuline glargine (Glargine) Onset: 3-4 hrs Peak: none Duration:10-24 hrs do not mix with other insulins

Explain the pathophysiologic process of hypoglycemia

Is low blood sugar less that 50-60 mg/dL. The brain is sensitive to low levels of blood glucose, so hypoglycemia has to be handled quickly. If blood sugar falls below the normal range, the brain will trigger the adrenal glands to release epinephrine. Glucagon will also be released from the pancreas and growth hormone will be released from the pituitary gland. All of these responses trigger release of sugar into the blood by the liver.

what affect doe hypoglycemia have on nervous tissue (brain)?

It can cause brain death or brain dysfunction

Glucophage

Metformin

The nurse is preparing a patient for a computed tomography scan using iodine contrast media. Which medication should the nurse question if prescribed one day before the scheduled procedure?

Metformin (Glucophage)

Describe the etiologies and pathophysiology of the following common chronic complications of diabetes mellitus: -Neuropathies -Nephropathies -Retinopathies -Macrovascular complications -Diabetic foot ulcers -Infections

NEUROPATHIES Diabetic neuropathy is a type of nerve damage that can occur if you have diabetes. Depending on the affected nerves, symptoms of diabetic neuropathy can range from pain and numbness in your legs and feet to problems with your digestive system, urinary tract, blood vessels and heart. NEPHROPATHIES Diabetic nephropathy is a serious kidney-related complication of type 1 diabetes and type 2 diabetes. It is also called diabetic kidney disease. Up to 40 percent of people with diabetes eventually develop kidney disease. RETINOPATHIES Retinopathy is any damage to the retina of the eyes die to diabetes, which may cause vision impairment. Retinopathy often refers to retinal vascular disease, or damage to the retina caused by abnormal blood flow. MACROVASCULAR COMPLICATIONS Diabetes causes things like coronary artery disease, peripheral arterial disease, and stroke. DIABETIC FOOT ULCERS A diabetic foot ulcer is an open sore or wound and is commonly located on the bottom of the foot. INFECTIONS Although not specifically an acute or a chronic complication, infections are a common concern of people with diabetes. Certain types of infections occur with increased frequency in people with diabetes: soft tissue infections of the extremities, osteomyelitis, urinary tract infections and pyelonephritis, candidal infections of the skin and mucous surfaces, dental caries and periodontal disease, and tuberculosis. Moreover, infections often are more serious in people with diabetes. Suboptimal response to infection in a person with diabetes is caused by the presence of chronic complications, such as vascular disease and neuropathies, and by the presence of hyperglycemia and altered neutrophil function. Sensory deficits may cause a person with diabetes to ignore minor trauma and infection, and vascular disease may impair circulation and delivery of blood cells and other substances needed to produce an adequate inflammatory response and effect healing. Pyelonephritis and urinary tract infections are relatively common in persons with diabetes, and it has been suggested that these infections may bear some relation to the presence of a neurogenic bladder or nephrosclerotic changes in the kidneys. Hyperglycemia and glycosuria may influence the growth of microorganisms and increase the severity of the infection. Diabetes and elevated blood glucose levels also may impair host defenses such as the function of neutrophils and immune cells. Polymorphonuclear leukocyte function, particularly adherence, chemotaxis, and phagocytosis, is depressed in persons with diabetes, particularly those with poor glycemic control.

HHS(HYPERGLYCEMIC HYPEROSMOLAR NONKETOTIC SYNDROME

NO ACIDOSIS/KETONES ARE NOT BROKEN DOWN "appears like a stroke"--char HHS-characterized by hyperglycemia (blood glucose>600mg/dl).. mostly affected type 2 diab pts

Intermediate acting insulin

NPH insulin (Humulin N) Onset: 1-2 hrs Peak: 4-12 hrs Duration: 18-24 hrs

Risk for cardiovascular disease and stroke

Over time the high glucose weaken the vessels and make patient more susceptible

Pramlintide (Symlin) is prescribed as supplemental drug therapy to the treatment plan for a patient with type 1 diabetes mellitus. What information should the nurse include when teaching the patient about the action of this medication?

Pramlintide slows gastric emptying.

Discuss the risk factors for gestational diabetes mellitus.

Pregnant women who are: -overweight -related to someone who has diabetes -are Hispanic/Latina, African American, American India, Alaska Native, Asian American, or a Pacific Islander -older than 25

Which insulin can be administered by continuous intravenous (IV) infusion?

Regular insulin (Humulin R)

short acting insulin

Regular insulin (Humulin R) Onset: 30 mins-1 hour Peak:2-4 hrs Duration: 5-7 hrs

Which information should the nurse include in a teaching plan for patients taking oral hypoglycemic drugs?

Report symptoms of anorexia and fatigue and advise to avoid smoking and alcohol consumption

Which actions describe the beneficial effects produced by sulfonylurea oral hypoglycemics?

Stimulate insulin secretion from beta cells, Enhance action of insulin in various tissues, and Inhibit breakdown of insulin by liver

Compare the Somogyi Effect to the Dawn Phenomenon.

The Somogyi effect describes a cycle of insulin-induced posthypoglycemic episodes. In people with diabetes, insulin-induced hypoglycemia produces a compensatory increase in blood levels of catecholamines, glucagon, cortisol, and growth hormone. These counterregulatory hormones cause blood glucose to become elevated and produce some degree of insulin resistance. The cycle begins when the increase in blood glucose and insulin resistance is treated with larger insulin doses. The hypoglycemic episode often occurs during the night or at a time when it is not recognized, rendering the diagnosis of the phenomenon more difficult. Research suggests that even mild insulin-associated hypoglycemia, which may be asymptomatic, can cause hyperglycemia in people with type 1 diabetes through the recruitment of counterregulatory mechanisms, although the insulin action does not wane. A waning of insulin's effects when it occurs (i.e., end of the duration of action) causes an exacerbation of the posthypoglycemic hyperglycemia that occurs and accelerates its development. These findings may explain the labile nature of the disease in some people with diabetes. Measures to prevent hypoglycemia and the subsequent activation of counterregulatory mechanisms include a redistribution of dietary carbohydrates and an alteration in insulin dose or time of administration. The dawn phenomenon is characterized by increased levels of fasting blood glucose, or insulin requirements, or both, between 5 am and 9 am without antecedent hypoglycemia. It occurs in people with type 1 or type 2 diabetes. It has been suggested that a change in the normal circadian rhythm for glucose tolerance, which usually is higher during the latter part of the morning, is altered in people with diabetes. Growth hormone has been suggested as a possible factor. When the dawn phenomenon occurs alone, it may produce only mild hyperglycemia, but when it is combined with the Somogyi effect, it may produce profound hyperglycemia. [SOMOGYI EFFECT: HYPOGLYCEMIA IN THE LATE EVENING CAUSES HYPERGLYCEMIA IN THE EARLY MORNING.] [DAWN PHENOMENON: JUST HYPERGLYCEMIA IN THE MORNING.]

Describe the etiologies, pathophysiology, and acute complications of hyperglycemic hyperosmolar state.

The hyperglycemic hyperosmolar state (HHS) is characterized by hyperglycemi , hyperosmolarity, and dehydration, the absence of ketoacidosis, and depression of the sensorium. Hyperglycemic hyperosmolar state may occur in various conditions, including type 2 diabetes, acute pancreatitis, severe infection, myocardial infarction, and treatment with oral or parenteral nutrition solutions. It is seen most frequently in people with type 2 diabetes. A partial or relative insulin deficiency may initiate the syndrome by reducing glucose utilization while inducing a glucagon-stimulated increase in hepatic glucose output. With massive glycosuria, obligatory water loss occurs. If the person is unable to maintain adequate fluid intake because of associated acute or chronic illness or has excessive fluid loss, dehydration develops. As the plasma volume contracts, renal insufficiency develops and the resultant limitation of renal glucose losses leads to increasingly higher blood glucose levels and an increase in severity of the hyperosmolar state. In hyperosmolar states, the increased serum osmolarity has the effect of pulling water out of body cells, including brain cells. The condition may be complicated by thromboembolic events arising because of the high serum osmolality. The most prominent manifestations are weakness, dehydration, polyuria, neurologic signs and symptoms, and excessive thirst. The neurologic signs include hemiparesis, Babinski reflex, aphasia, muscle fasciculations, hyperthermia, hemianopia, nystagmus, visual hallucinations, seizures, and coma. The onset of HHS often is insidious, and because it occurs most frequently in older people, it may be mistaken for a stroke. [A COMPLICATION OF DIABETES MELLITUS IN WHICH HIGH BLOOD SGUAR RESULTS IN HIGH OSMOLARITY WITHOUT SIGNIFICANT KETOACIDOSIS.]

Describe the etiology, pathophysiology, clinical manifestations, and the specific role metabolic syndrome plays in the development of Type II diabetes mellitus: metabolic abnormalities.

The metabolic abnormalities involved in type 2 diabetes include (1) insulin resistance, (2) increased glucose production by the liver, and (3) impaired secretion of insulin by the pancreatic beta cells. Insulin resistance, which can be defined as the failure of target tissues to respond to insulin, predates the development of hyperglycemia. That is, in the early stages of the evolution of type 2 diabetes, insulin resistance is usually accompanied by compensatory beta cell hyperfunction and hyperinsulinemia. In skeletal muscle, insulin resistance prompts decreased uptake of glucose. Although muscle glucose uptake is slightly increased after a meal, the efficiency with which it is taken up (glucose clearance) is diminished, resulting in an increase in postprandial (following a meal) blood glucose levels. In contrast, in the liver, insulin resistance leads to impaired suppression of glucose production with an overproduction of glucose despite a fasting hyperinsulinemia. In fact, the excessive rate of hepatic glucose production is the primary determinant of elevated FPG in persons with type 2 diabetes. Several mechanisms can lead to impaired secretion of insulin by the pancreatic beta cells. These include an initial decrease in beta cell mass related to genetic or epigenetic factors, increased apoptosis or decreased regeneration of beta cells, or beta cell exhaustion due to long-standing insulin resistance. According to one study, beta cell function was reduced by an average of 50% at the time of diagnosis in type 2 diabetes, and progressively decreased resulting in worsening hyperglycemia even when the degree of insulin resistance remained stable.

Explain the pathophysiology of diabetes mellitus.

The pancreas is supposed to produce and secrete insulin. Insulin is required to move glucose out of the vascular space and into the cell. If the glucose is not pulled from the vascular space, it will build up in the blood. The cells need the glucose for energy. Without insulin, the body enters a state of catabolism which means it starts to tear down the body. The cells need energy, so thy start breaking down fats and proteins. FAT breakdown leads to ketone formation. Ketones are acids. The increase in ketones in the blood leads to metabolic acidosis. DM type I begins in chilldhood or adolescence and is when the pancreas does not function properly and does not produce insulin at all. Even if the patient takes medication to stimulate production, the pancreas just will not do it. The patient has to take insulin hormone replacements. DM type II is more common and is related to obesity. It usually occurs after the age of 30 and is most commonly seen between the ages of 50-60. This is a nonketonic form of DM because there is enough insulin produced to prevent the breakdown of fats. These patients do not have enough insulin or the insult they have does not work correctly at the cellular level (which is called insulin resistance). The pancreas works correctly, it just does not work enough or the patient is taking in so much glucose that the pancreas can not keep up. There is a genetic disposition for DM type II but other factors include obesity, dietary intake, and environmental factors.

Describe the etiology, pathophysiology, clinical manifestations, and the specific role metabolic syndrome plays in the development of Type II diabetes mellitus: insulin resistance.

There is increasing evidence to suggest that when people with type 2 diabetes present predominantly with insulin resistance, the diabetes may represent only one aspect of a syndrome of metabolic disorders. Hyperglycemia in these people is frequently associated with intra-abdominal obesity, high levels of plasma triglycerides and low levels of high-density lipoproteins (HDLs), hypertension, systemic inflammation (as detected by C-reactive protein [CRP] and other mediators), abnormal fibrinolysis, abnormal function of the vascular endothelium, and macrovascular disease (coronary artery, cerebrovascular, and peripheral arterial disease). This constellation of abnormalities often is referred to as the insulin resistance syndrome, syndrome X, or, the preferred term, metabolic syndrome.

management of hypoglycemia

Treat with 10-15 g of simple carb (1 tbs sugar) Ex: 15 g of carbs= 4 oz OJ, 8 oz milk, 3-4 tabs of glucose tabs , 4 oz soft drinks Monitor glucose again follow with complex carb IF child is unconscious or unable to swallow: admin glucagon SC or IM and admin simple carb as soon as tolerated

amylin levels

increase in response to nutritional stimuli that leads inhibition of gastric emptying & glucagon secretion

Describe the etiology, pathophysiology, and clinical manifestations of Type I diabetes mellitus.

Type 1 diabetes mellitus, which is characterized by destruction of the pancreatic beta cells and accounts for 5% to 10% of those with diabetes, is subdivided into type 1A immune-mediated diabetes and type 1B idiopathic (non-immune-related) diabetes. In the United States and Europe, approximately 90% to 95% of people with type 1 diabetes mellitus have type 1A immune-mediated diabetes. The rate of beta cell destruction is quite variable, being rapid in some individuals (mainly infants and children) and slow in others (mainly adults). Some individuals, particularly children and adolescents, may present with diabetic ketoacidosis (DKA) as the first manifestation of the disease. Others may have modest elevations in FPG that can rapidly change to severe hyperglycemia and DKA in the presence of stress and infection. Still others, particularly adults, may retain sufficient beta cell function to delay onset of clinical diabetes for many years. The destruction of beta cells and absolute lack of insulin in people with type 1 diabetes mellitus mean that they are particularly prone to the development of DKA. One of the actions of insulin is the inhibition of lipolysis (i.e., fat breakdown) and release of free fatty acids (FFAs) from fat cells. In the absence of insulin, ketosis develops when these fatty acids are released from fat cells and converted to ketones in the liver. Because of the loss of insulin response, all people with type 1A diabetes require exogenous insulin replacement to reverse the catabolic state, control blood glucose levels, and prevent ketosis. Diabetes mellitus may have a rapid or an insidious onset. In type 1 diabetes, signs and symptoms often arise suddenly. The most commonly identified signs and symptoms of diabetes are often referred to as the three polys: (1) polyuria (i.e., excessive urination), (2) polydipsia (i.e., excessive thirst), and (3) polyphagia (i.e., excessive hunger). These three symptoms are closely related to the hyperglycemia and glycosuria of diabetes. Weight loss despite normal or increased appetite is a common occurrence in people with uncontrolled type 1 diabetes. Other signs and symptoms of hyperglycemia include recurrent blurred vision, fatigue, paresthesias, and skin infections. [A CHRONIC CONDITION IN WHICH THE PANCREAS PRODUCES LITTLE OR NO INSULIN RESULTING IN HIGH BLOOD SUGAR LEVELS IN THE BODY.]

Hypoglycemia

abnormally low level of sugar in the blood:main mx**HEADACHE**

postprandial

after a meal

which cells secrete glucagon?

alpha cells of pancreas

type 2 diabetes

cellular resistance to insulin with or without beta cell exhaustion (90%-95%) can need insulin or not

what does the liver do in the body

controls storage & mobilization of the body's fuel supply

somogyi effect

cycle of insulin-induced post hypoglycemic episodes; 'hypoglycemia begets hyperglycemia'; see compensatory increase in glucagon, epinephrine, cortisol & GH with development of hyperglycemia

risks factors for hypoglycemia

diabetes excess insulin/orgal hypoglycemics not enough food excess physical activity alcohol intake

somatic neuropathy

distal symmetric polyneuropathy in which loss of function typically occurs in stocking-glove pattern

Fats

energy source -turned into triglycerides & stored in adipose tissue

hormones that affect glucose levels

epinephrine, growth hormone, glucocorticoid hormone

what is normal blood glucose levels?

fasting: 70-100 after carb-containing meal: normally rises to 200

proteins

for creation of all body structures -including enzymes, genes, muscles, matrix, bone, hemoglobin of red blood cells

gluconeogenesis

formation of glucose from non-carbohydrates

Glycogenesis

formation of glycogen from glucose

what do the brain and nervous system rely on as fuel

glucose -the brain cannot store or synthesize glucose so it is needed on a daily basis

what does the body use to satisfy their energy needs?

glucose, fatty acids

What does glucagon promote?

glycogenolysis and gluconeogenesis

epinephrine

help maintain during stress. increase glucose levels, increase glycogenolysis, increase breakdown of fat (lipolysis), iinhibit secretin of insulin from beta cells

insulin

hormone that helps blood glucose enter the cells for storage used in Type I and in many cases of Type II Diabetes Mellitus 5 types: 1. short acting - begins 30 min after injection lasting 5-8 hours 2. rapd acting - rapid onset typically administered before a meal 3. intermediate to long acting - slower onset and longer duration 4. multiple daily injections (MDI) 5. Continuous SubQ insulin Infusion (CSII) A hormone secreted by the islets of Langerhans in the pancreas that regulates the amount of glucose in the blood

Somogyi effect

hypoglycemia followed by rebound hyperglycemia

Type 1 B diabetes mellitus

idiopathic beta cell destruction with no evidence of autoimmunity

glucagon functions

increase blood glucose levels and you will see a rise in levels by not eating all day. Functions: Increase glycogenolysis(breakdown of glycogen), increase gluconeogenisis(production of glucose from sugar), increase lipolysis (breakdown of fat)

growth hormone

increase during exercising or fasting. increase glucose levels, decrease uptake of insulin

insulin functions

increase glycogenisis (production of glucose form sugar), decrease glycogenolysis(the breakdown of glycogen to form glucose for energy), decrease lipolysis (breakdown of fat), increase lipogenesis(production of fat), increase protein sythesis, inhibit gluconeogenesis (formation of glucose from non carbohydrates)

organs response to insulin deficiency

lipolysis of storage fat and release of FFA

rapid acting insulin

insulin lispro (Humalog) Onset: less than 15 mins Peak: 30 mins-1 hr Duration:3-4 hrs

what happens if there is excess glucose & glycogen

it is transformed into fatty acids & stored as triglycerides in the fat cells

Where is glycogen stored in the body?

liver and muscles

neuropathies

loss of feeling or sensation in extremities usually in diabetics cause by decrease blood flow to the nerve cells. You will lose the myelin sheath(so nerve cell dont work as fast

glucagon and insulin

pancreatic hormones

exocrine acini tissue

secretes digestive juices into the duodenum

glycogenolysis

the breakdown of glycogen to form glucose for energy

Obesity and inactivity can increase the chances of forming what type of diabetes?

type 2