Diabetes Mellitus 2

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Exogenous Insulin

______: must be injected- Required for type 1 diabetes; and may be needed for the patient with Type 2 diabetes who cannot control blood glucose by other means.

Human insulin

Types of Insulin: ________- genetically engineered to be like human insulin. Animal insulin is more expensive, and have parts that are not useful to humans. Most widely used type of insulin. Decreased likehood of allergic reaction.

Insulins differ

______ in regard to onset, peak action, and duration. Varies in each person, Poor kidney function will last longer and increases risk of hypoglycemia.

Different types

_______ of insulins may be used for combination therapy. -Rapid acting: Laspro (Humalog), Aspart (Novolog), Glalister (Aspida), Exubera. -Short acting: Regular. Intermediate acting: NHP or Lente. Long acting: Lantus (Glaritus) , Levimir (Delemir).

Administration of insulin

Cannot be taken orally. SQ injection for self-administration. IV administration: use regular. Lantus cannot be mixed with any other insulins. Insulin can be stored at room temperature for up to one month. Flocculation of insulin: NPH molecule remain in clumps...wont work if this occurs.

Basal Insulin

Insulin Management: ________- Baseline insulin required to maintain normal glucose volumes while fasting between meals.

Bolus insulin

_______ (meal _____): occurs with meals, insulin required to curve the raise in the blood glucose following a meal.

Conventional Therapy

______: attempt to mimic normal body regulation of insulin. NHP and Regular (R/P). insulin. -N/R one injection/day: usually 30 mins before someone eats breakfast- Regular effects breakfast, NPH effects lunch and Hyperglycemia around dinner.

Somogyi effect

-NPH given at dinner peaks in the middle of the night causing a increase in blood glucose. Body Counterregulatory hormones are released causing blood glucose to rise. Care provider may increase dinner NPH, causing more severe nocturnal hypoglycemia and possibly higher FBS.

Somogyi effect: Solution

_________- Test 2-3 am glucose. If low, then move NPH to at bedtime, so that peak of NPH is shifted to later in early morning.

Dawn Phenomenon

______: Release of growth hormone, cortisol, glucagon between 4am - 11am contribute to: an increase in blood glucose. NPH given at dinner time is waning in action, and therefore will not control rise in blood glucose.

Dawn phenomenon: Solution

______: Test blood glucose 02-03. If it is normal, and FBS is elevated, the rise in blood glucose is likely related to Dawn Phenonomenon. Solution is the same: move NPH to bedtime.

Dawn phenomenon: Solution

______: The action of the NPH insulin given at Dinner time poops out before morning--- There is no basal insulin left in the system, and the blood sugar naturally rises...______ move NHP to bedtime.

Conventional Therapy

-N/R twice a day: Same as 1 injections but dinner is covered along with fasting blood glucose.

Conventional Therapy

-N/R 3 injections/day: NPH and Regular, Regular, and NPH later in the evening.

Basal/Bolus

______: MDI= multiple dose injections. Baseline insulin and at meal time insulin. Fasting insulin provides both basal and bolus coverage.The pump more closely stimulates the physiological fueling of the pancreas, increases flexibility in lifestyle.

N + Log

Humalog is right before a meal, after a meal, great for children and Elderly.

Carbohydrate Counting

Allows someone with diabetes to match insulin to food eaten, rather than eating to feed insulin.

Carbohydrate

_____: Starches- 15 g of ____ in one serving; Fruits/Juices- 15g of ____ in one half cup; Milk- 12 g of ____ in one serving; Honey, Table sugar, syrup and candy

Why use

____ Carbohydrate counting with intensive therapy? It is very accurate and is customized for each patient. Matches insulin to food eaten. Gives more flexibility in food choices. It is easy to understand and use for most patients.

Why do

_____ Carbohydrates get all of the attention? -90-100% of carbohydrates that are injected are converted to 100% glucose in 15-90 minutes after eating.

Protein

_______: ONLY 50-60% of _____ is converted to glucose and the percentage of fat is even less.

Premeal bolus

______ stated in terms of...1 unit/XX grams of carbohydrate; 1 unit of insulin will metabolize xx grams of carbohydrate.

Meal bolus

Determining a ______: Patient determines doseage amount based on: Blood glucose value (correction bolus); and Carbohydrates in meal or snack (Meal bolus).

Correction bolus

______: insulin required to return an increase blood glucose to a goal.

Insulin Sensitivity Factor

______ (ISF): Also called correction factor: how much one unit of insulin will lower the blood glucose (different for each patient).

Bolus Insulin

_____: amount given pre-meal, depends on...glucose goal, premeal blood glucose, insulin sensitivity factor (ISF).

Insulin Therapy: Disadvantages

______: You gotta inject it- hurt (insulin doesn't hurt). Hypoglycemia- if insulin is not managed correctly. Lipodystrophy: stop injecting in those sites, it may go away isn't painful.

Where to inject

Insulin Therapy: ______- Most rapid to least rapid insulin absorption: Abdomen, arms, thighs, buttocks. In Lantus doesnt matter where you apply. Pattern rotation: rotate within injection sites, rather than rotating to a different area with each injection. May decrease variability in absorption from day to day.

Insulin use

_____ in Type 2 Diabetes: Often used in the following situations: Hyperglycemia despite maxial dose of oral agents; Allergy to oral agents; Serioud infection; Pregnancy: stressful; Surgery: stressful; and Renal failure.

Insulin Use: Disadvantages

_____ in Type 2 Diabetes: _____- Hypoglycemia most common side effect; Weight gain; Patient concerns; Large insulin doses often require for optimal control; Multiple injections usually required (compliance issue).

Other drugs affecting

DM Drug therapy: _______ blood glucose levels: -Beta-Adrenergic blockers: (HTN) hypoglycemic unawareness. -Thiazide: may potentiate hyperglycemia. -Loop diuretics: may potentiate hyperglycemia.

Nursing Assessment

Nursing Management: _______- Past health history, Viral infections, Medications, Recent surgery, Positive health history, Obesity, Weight loss, Thirst, Hunger, Poor healing, Kussmauls resp: Deep and rapid with a fruity odor.

Nursing Diagnoses

Nursing Management: ________- Ineffective therapeutic regiment management, Risk for injury, Risk for infection, Powerlessness, Imbalanced nutrition: More than body requirement, and Fluid Volume Deficit.

Planning

Nursing Management: ________- Overall goals, Active paitent participation, Few or no episodes of acute hyperglycemic emergencies or hypoglycemia, Maintain normal blood glucose levels, Prevent or delay chronic complications, and Lifestyle adjustments with minimal stress.

Ambulatory and home care

Nursing Implementation: _________- Overall goal is to enable patient or caregiver to reach an optimal level of independence. Insulin therapy and oral agents: Education on proper administration, adjustment adn side effects; Assessment of patient's response to therapy.

Personal hygiene

Nursing Implementation: _______- Regular bathing and emphasis on foot care; Daily brushing/flossing; Dentist should be informed about diabetes diagnosis.

Medical identification

Nursinf Implementation: ________ and travel card- Must carry identification indicating diagnosis of diabetes.

Patient and Family teaching.

Nursing Implementation: _______- Educate on disease process, physical activity, medications, monitoring blood glucose, diet, and resources; Enable patient to become most active participant in his/her care.

Evaluation

Nursing management: ______- Knowledge, Balance of nutrition, Immune status, Health benefits, No injuries.

Acute

Diabetes Complications: _____- Hypoglycemia: defined as any blood glucose level of < 70 mg/dl.

Mild Hypoglycemia

______- Characteristics: Sweating, trembling, difficulty concentrating, light headiness, the client can treat themselves.

Severe Hypoglycemia

______- Characterized by inability to treat themselves do to mental confusion, lethargy or unconsciousness.

Symptoms

_______ of Hypoglycemia- Type 1 & 2 are the same. Recurrent hypoglycemic experiences can cause hypoglycemic unawareness: Blunt there symptoms. Medications (beta blockers) can cause hypoglycemia unawareness. Autonomic: Trembling/shaking, Sweating. Neuoglycopenic: Slurred speech, clammy, fatigue sleepiness, and trouble concentrating.

Rule of 15

Treatment of mild hypoglycemia: _______- BG 50-70 mg/dl: with 10-15 grams of carbs. BG <50, with 20-30 grams of carbs. Recheck BG, if BG <70 retreat with 10-15 gram of carb. Wait 15 mins, repeat.

Assure patient safety

Treatment of severe hypoglycemia: _______- Individualized based on patient status. Conscious cooperative: 15-30 grams of carbs rule of 15 still applies. Conscious but uncooperative: Glucagon injection. Unconscious: Glucagon, sugar to buccal tissue. IV push of Glucose.

Glucagon

_____: 1 mg kit that every PWD who is on insulin should have in their house, at work, where ever!!!!! (Takes 10 mins to make and once mixed it is only good for 24 hours.)

Glucagon Rules

______: Kept in the same place. Significant other should be familiar with giving injections so that when duty calls, they con do the job. Roll client to side after administering, as may cause nausea/vomiting.

Sick day guidelines

DM Acute Complications: _______- Physiological stress can contribute to elevated blood glucose. Continue with regular meal plan. Increase non calorie fluids (hydration). With nausea/vomiting may need substitute solid food with calories-containing fluids: soups, juices, and regular decaffeinated soft drinks.

Sick day guidelines

DM Acute Complications: _______- Contact HCP if unable to keep food down. Continue taking insulin/oral agents. Test BG at least every 2-4 hours. Urine ketone testing if BG >240 mg/dl. Contact HCP if blood glucoses elevated.

Diabetic Ketoacidosis (DKA)

Caused by profound deficiency of insulin.

Characterized by

DKA _______- Hyperglycemia, ketosis, acidosis, dehydration, and mostly occurs in Type 1.

Precipitating factors

DKA _______- Illness, Infection, Inadequate insulin dosage, Undiagnosed Type 1, Poor self-management, and Neglect.

Pathophysiology

DKA: ______- When supply of insulin insufficient, glucose cannot be properly used for energy. Body breaks down fat stores.

Leathargy/weakness

DKA S/S: _______- Early symptoms. Dehydration: Poor skin turgor, dry mucous membranes, tachycardia, orthostatic hypotension.

Ketones

DKA S/S- ______ are by-products of fat metabolism: Alter pH balance, causing metabolic acidosis, Ketones bodies excreted in urine, and Electrolytes become depleted.

Abdominal pain

DKA S/S- ______: Nausea/Vomiting

Kussmaul respirations

DKA S/S- ______: Rapid deep breathing, Attempt to reverse metabolic acidosis- Sweet fruity odor

Serious condition

DKA S/S- _______: Must be treated promptly, and Depending on S/S may or may not need hospitalization.

Laboratory findings

DKA ______- Glood glucose >300 mg/dl. Arterial blood pH below 7.30. Serum bicarbonate level < 15 mEq/L. Ketones in blood and urine.

DKA treatment

_____- Correct fluid/electrolyte imbalance: IV infusion 0.45% or 0.9% NaCl (isotonic), Restore urine output, and Raise blood pressure.

Insulin therapy

Withheld until fluid resuscitation has begun. Bolus followed by insulin drip. When blood glucose levels approach 250 mg/dl 5% dextrose added to regimen- Prevent hypoglycemia. Postassium replacement- Cardiac monitoring.

Hyperomolar Hyperglycemic Syndrome

_______- Life-threatening syndrome. Less common than DKA. Often occurs in patients over 60 years with type 2. Patient has enough circulating insulin so ketoacidosis does not occur. Produces fewer symptoms in earlier stages. Neurologic manifestations occur due to increase serum osmolality.

Usually history of

HHS- ______: Inadequate fluid intake. Increasing mental depression. Polyuria.

Medical Emergency

HHS- _______: High mortality rate. Therapy similar to DKA. Except HHS requires greater fluid replacement.

Laboratory values

HHS- ______: Blood glucose > 400 mg/dl. Increase in serum osmolality. Absent/minimal ketone bodies.

Nursing management

______ DKA/HHS- Patient closely monitored. Administration- IV fluids, Insulin therapy, and Electrolytes. Assessment. Renal status. Cardiopulmonary status. LOC. Signs potassium imbalance. Cardiac monitoring. VS.

Chronic Complications

DM _____: General concept. _____ can be avoided and slowed by managing the "Hypers" Hyperglycemia, Hypertension and Hyperlipidemia- and add smoking to the list.

Macrovascular

Angiopathy: _______- Diseases of large and medium sized blood vessels. Occur with greater frequency and with an earlier onset in diabetic.Development promoted by altered lipid metabolism common to diabetes. tight glucose control may delay artherosclerotic process.

Macrovascular risk factors

__________- Obesity. Smoking. Hypertension. High-fat intake. Sedentary lifestyle. Patients with diabetes should be screened for dylipidemia at diagnosis.

Microvascular

Angiopathy: _______- Is specific to PWD. Results from thickening of vessel membranes in capillaries and arterioles. In response to chronic hyperglycemia. Areas most noticeably affected- Eyes (retinopathy) and Kidneys (Diabetic ephropathy)

Retinopathy

Eyes (________)- Micovascular damage to retina. Result of chronic hyperglycemia. Most common cause of new cases of blindness in people 20 to 74 years.

Nonproliferative

Retinopathy: ________- Most common form. Partial occlusion of small blood vessels in retina...Causes development of microaneurysms.

Proliferative

Retinopathy: ______- Most severe form. -Involves retina and vitreous. -When retinal capillaries become occluded: Body form new blood vessels, Vessels are extremely fragile and hemorrhage easily, Produce vitreous contraction, and Retinal detachment can occur.

Earliest

______ and most treatable stages often produces no changes in vision. -Annual eye exams by ophthalmologist.

Treatment

Microvascular- _______: Laser photoagulation: destroys the ischemic areas of the retina that encourage neovascularization. Vitrectomy- Aspiration of blood, membrane, fibers from inside eye through small incision.

Diabetic nephropathy

Kidneys: _______- Associated with damage to small vessels that supply the glomeruli of the kidney. Leading cause of end-stage renal diesase.

Diabetic nephropathy

Kidneys: ______- Critical factors for prevention/delay: Tight glucose control, Blood pressure management, Angiotensin-converting enzyme (ACE) inhibitors: Used even when not hypertensive and Angiotension II receptor antagonists. -Yearly screening. Microalbuminuria in urine. Serum creatinine. Chronic complications.

Diabetic neuropathy

60% to 70% of PWD have some degree of neuropathy. Nerve damage due to metabolic derangements of diabetes.

Sensory neuropathy

Distal symmetric: Most common form, affects hands and/or fett bilaterally, Characteristics include...Loss of sensation, abnormal sensations, pain and parethesias; Usually worse at night; Foot injusty and ulcerations can occur w/o the pt having any pain. Can cause atrophy of small muscles of hands/feet.

Sensory neuropathy- Treatment

Tight blood glucose control- Drug therapy, Topical creams, Tricyclic antidepressants, and Antiseizure medications.

Autonomic

Can affect nearly all body systems and complications: Gastroparesis- Delayed gastric emptying; Cardiovascular abnormalities; Sexual function; Neurogenic bladder.

Foot and Lower extremity

Complications of _______: Foot complications. Most common cause of hospitalizations in diabetes. Result from combination on microvascular and macrovascular diseases.

Risk factors

Complications of foot and lower extremity: _______- Semsory neuropathy and Peripheral arterial disease.

Other contributors

Complications of foot and lower extremity: ______- Smoking, Clotting abnormalities, Impaired immune function, Autonomic neuropathy.

Feet problems

Increased risk of _________: Decreased sensation, impaired micro and microvascular function all work together to cause problems that impact quality of life and cost a bunch of dollars.

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