Learning Outcomes Theory

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Patho Type 2 Diabetes
The pancreas tends to continue to produce endogenous (self-made) insulin. However, the insulin that is produced is either not enough or the tissues do not use it properly (or both). The presence of endogenous insulin is the major difference between type 1 & 2.
Insulin resistance refers to when cells of the body such as the muscle, liver and fat cells fail to respond to insulin, even when levels are
Common manifestations of uncontrolled type diabetes
Fatigue, recurrent infections, recurrent vaginal yeast or candidal infections, prolonged wound healing, and visual changes.
Chronic complications of type 2 diabetes
Long-term complications of type 2 are diabetic retinopathy, kidney disease (nephropathy), diabetic neuropathy, and macrovascular problems.
Type 2 diabetes can also affect the large blood vessels, causing plaque to eventually build up and potentially leading to a heart attack, stroke or vessel blockage in the legs (peripheral vascular disease).
Microvascular complications:
diabetic retinopathy
Diabetic retinopathy is a diabetes complication that affects eyes. It's caused by damage to the blood vessels of the light-sensitive tissue at the back of the eye (retina). At first, diabetic retinopathy may cause no symptoms or only mild vision problems. Eventually causing blindness.
Diabetic Nephropathy
Diabetic kidney disease, or diabetic nephropathy, is a complication of type 1 or type 2 diabetes caused by damage to the kidneys' delicate filtering system. Your kidneys contain millions of tiny blood vessel clusters (glomeruli) that filter waste from your blood. Can lead to kidney failure.
Diabteic Neuropathy
Diabetic neuropathy is a type of nerve damage that can occur if you have diabetes. High blood sugar can injure nerve fibers throughout your body, but diabetic neuropathy most often damages nerves in your legs and feet.
Depending on the affected nerves, symptoms of diabetic neuropathy can range from pain and numbness in your extremities to problems with your digestive system, urinary tract, blood vessels and heart. For some people, these symptoms are mild; for others, diabetic neuropathy can be painful, disabling and even fatal.
Uncontrolled hypertension in diabetic person
High blood pressure, or hypertension, is a condition that often affects people with type 2 diabetes. It is unknown why there is such a significant correlation between the two diseases, but it is widely assumed that obesity, a high-fat, high-sodium diet, and inactivity have led to a rise in both conditions.
According to the ADA, the combination of hypertension and type 2 diabetes is particularly lethal and can significantly raise a person's risk of having a heart attack or stroke. Having type 2 diabetes and high blood pressure also increases your chances of developing other diabetes-related diseases, such as kidney disease, and retinopathy (eye blood vessels), which may cause blindness.
Oral agents used in the treatment of type 2 in terms of mechanisms of action
Biguanide (metformin): Reduce glucose production by the liver
Sulfonylureas (glipizide) Increase insulin production in thepancreas
Meglitinides (nateglinide): Increase insulin production by the pancreas
Alpha-Glucosidase Inhib (acarbose): Starch-blockers: delay absorption of glucose from GI tract
Thiazolidinediones (pioglitazone): Increase glucose uptake in muscle; decrease endogenous glucose production
Dipeptidyl Peptidase-4 (linagliptin): Enhance activity of incretins, stimulate release of insulin from pancreatic beta cells, decrease hepatic glucose production
Oral agents used in treatment of type 2 in terms of side-effects
Biguanide (metformin): diarrhea, lactic acidosis
Sulfonylureas (glipizide): weight gain, hypoglycemia
Meglitinides (nateglinide): weight gain, hypoglycemia
Alpha-Glucosidase Inhib (acarbose): gas, abdominal pain, diarrhea
Thiazolidinediones (pioglitazone): weight gain, edema,
Dipeptidyl Peptidase-4 (linagliptin): pancreatitis, allergic reactions
Oral agents used in the treatment of type 2 in terms of metabolic effects
Biguanide (metformin): duration: 12 and 24 hr.
Sulfonylureas (glipizide): duration: 24 hr, LA
Meglitinides (nateglinide): duration 4 hr. intermediate
Alpha-Glucosidase Inhib (acarbose): duration: unknown short-acting
Thiazolidinediones (pioglitazone): duration 24 hr, long-acting
Dipeptidyl Peptidase-4 (linagliptin): duration 24 hr, LA
Oral agents used in the treatment of type 2 in terms of side effects and contraindications.
Biguanide (metformin): diarrhea, lactic acidosis
Sulfonylureas (glipizide): weight gain, hypoglycemia
Meglitinides (nateglinide): weight gain, hypoglycemia
Alpha-Glucosidase Inhib (acarbose): gas, abdominal pain, diarrhea
Thiazolidinediones (pioglitazone): weight gain, edema,
Dipeptidyl Peptidase-4 (linagliptin): pancreatitis, allergic reactions
Discuss hypoglycemia as a consequence of diabetes management, including causes, S/S, treatment and prevention.
Hypoglycemia may be caused by insulin or oral antidiabetic drug overdoses; failure to eat an adequate number of calories despite diabetic treatments; unusual levels of exercise (usually among treated diabetics); extreme starvation (fasting hypoglycemia); alcoholic depletion of carbohydrate reserves from the liver; salicylate overdoses; and rarely, an insulin-secreting tumor of the pancreas.
A patient with moderately low blood sugar may feel fatigued, dizzy, restless, hungry, or unusually irritable; have difficulty concentrating; or have spontaneous episodes of sweating, palpitations, tremor, or nausea. Severely low blood sugar produces delirium, violent behaviors, obtundation, seizures, coma, and, occasionally, death. Some patients who have treated their diabetes mellitus with insulin for many years may lose the normal ability to recognize symptoms of low blood sugar.
Hyperglycemia as a consequence of diabetes management, including causes, S/S, treatment and prevention.
Abnormally high blood sugar levels. Hyperglycemia can cause numerous unwanted effects. It can impair wound healing; decrease the body's ability to fight infections; worsen the neurological deficits found in stroke; increase the risk of death in critically ill patients; and damage the kidneys, peripheral nerves, retinae, blood vessels, and heart.
Hyperglycemia may result from damage to the insulin secreting cells of the pancreas; infusions of dextrose; insulin resistance; obesity; overeating; a sedentary lifestyle; the stress of heart attack or other critical illnesses; or treatment with some drugs such as steroids or protease inhibitors.
Among outpatients, high blood sugar levels can be reduced with caloric restriction (dieting), regular exercise, oral hypoglycemic agents, insulin, and/or withholding offending drugs. Self-blood glucose monitoring and the keeping of a blood sugar log helps patients and their health care providers to recognize and manage hyperglycemic trends. Patients with diabetes mellitus need to understand the role maintaining glycemic control plays in preventing complications of their disease. Consultation with a diabetic nurse educator can provide the necessary information (and impetus) for good management of diet, medication regimens, and exercise.
Difference between type 1 and type 2 diabetes
In type 1 diabetes, the body makes little or no insulin because beta cells that make insulin are destroyed by the immune system. So people with type 1 diabetes must take insulin every day. Type 1 diabetes usually occurs in children and young adults but can also appear in older adults.
In type 2 diabetes, your body may not make enough insulin, it doesn't respond to insulin properly (insulin resistance), or both. Most people with diabetes in the United States (about 90% to 95%) have type 2. This kind of diabetes usually occurs in people who are older or in those who are overweight. In fact, about 80% of people with type 2 diabetes are overweight.
Important teaching points in patient eduation
Patient teaching should include insulin training, Self-monitoring of blood glucose (SMBG), diet and nutrition, carb counting (if needed), exercise (how much or how little), fluid intake (what is good to drink), and alcohol intake.
Define dementia and describe its impact on society
Dementia is a syndrome characterized by dysfunction or loss of memory, orientation, attention, language, judgment, and reasoning. Personality changes and behavioral problems such as agitation, delusions, and hallucinations may result.
Dementia is overwhelming for the families of affected people and for their caregivers. Physical, emotional and economic pressures can cause great stress to families and caregivers, and support is required from the health, social, financial and legal systems.
Dementia has significant social and economic implications in terms of direct medical costs, direct social costs and the costs of informal care.
Describe the clinical manifestations, diagnostic studies, and collaborative management of dementia
Behavioral changes may include the following: Eating, dressing, toileting (e.g., unable to dress without help; becomes incontinent) Interests (e.g., abandons hobbies) Routine activities (e.g., unable to perform household tasks) Personality (e.g., inappropriate responses, lack of emotional control)
Multi-infarct dementia is the most common form of vascular dementia, which is a deterioration in mental function caused by narrowing of blood vessels in the brain.
Keeping a schedule, not too may options for the patient to choose from everyday, quiet environment
Describe the clinical manifestations, diagnostic studies, and collaborative management of AD
Alzheimer's disease (AD) is a chronic, progressive, degenerative disease of the brain. It is the most common form of dementia.
The exact etiology is unknown. Similar to other forms of dementia, age is the most important risk factor for developing AD. Multiple genetic factors have been linked to its development.
Characteristic findings relate to changes in the brain's structure and function: amyloid plaques, neurofibrillary tangles, and loss of connections between cells and cell death.
Describe the diagnostic studies, and collaborative management of AD
The stages of AD can be categorized as mild, moderate, and severe.
An initial sign is a subtle deterioration in memory. With progression of AD, additional cognitive impairments are noted, including dysphasia, apraxia, visual agnosia, and dysgraphia.
No single clinical test can be used to diagnose AD; the diagnosis is one of exclusion.
At this time there is no cure for AD. The collaborative management is aimed at improving or controlling decline in cognition and controlling the undesirable behavioral manifestations that the patient may exhibit.
Drug therapy may slow the worsening of symptoms but does not cure AD.
Describe the clinical manifestations, diagnostic studies, and collaborative management of MCI
Mild cognitive impairment (MCI) is a state of cognitive functioning that is below defined norms yet does not meet the criteria for dementia.
Causes of MCI may include stress, anxiety, depression, or physical illness.
The nurse caring for the patient with MCI must recognize the importance of monitoring the patient for changes in memory and thinking skills that would indicate a worsening of symptoms or a progression to dementia.
Describe the nursing management of the patient with a cognitive disorder
The diagnosis of AD is traumatic for both the patient and the family. It is not unusual for the patient to respond with depression, denial, anxiety and fear, isolation, and feelings of loss. The nurse is in an important position to assess for depression and suicidal ideation.
Currently, family members and friends care for the majority of individuals with AD in their homes. Others reside in various facilities, including long-term care and assisted living facilities.
The severity of the problems and the amount of nursing care intensify over time. As AD progresses to the late stages (severe impairment), there is increased difficulty with the most basic functions, including walking and talking. Total care is required.
Describe the etiology of delirium
Delirium occurs when the normal sending and receiving of signals in the brain become impaired. This impairment is most likely caused by a combination of factors that make the brain vulnerable and trigger a malfunction in brain activity.
Delirium may have a single cause or more than one cause, such as a medical condition and medication toxicity. Sometimes no cause can be identified. Possible causes include:

Certain medications or drug toxicity
Alcohol or drug abuse or withdrawal
A medical condition
Metabolic imbalances, such as low sodium or low calcium
Severe, chronic or terminal illness
Fever and acute infection, particularly in children
Exposure to a toxin
Malnutrition or dehydration
Sleep deprivation or severe emotional distress
Pain
Surgery or other medical procedures that include anesthesia
Describe the pathophysiology of delirium
Hypotheses about the pathophysiology of delirium are speculative and largely based on animal research. According to the neurotransmitter hypothesis, decreased oxidative metabolism in the brain causes cerebral dysfunction due to abnormalities of various neurotransmitter systems.
Describe the clinical manifestations of delirium
Clinically, delirium is rarely caused by a single factor. It is often the result of the interaction of the patient's underlying condition with a precipitating event.
Acute delirium occurs frequently in hospitalized older adults. This transient condition is characterized by disorganized thinking, difficulty in concentrating, and sensory misperceptions that last from 1 to 7 days.
Manifestations of delirium are sometimes confused with dementia. A key distinction between delirium and dementia is that the person who exhibits sudden cognitive impairment, disorientation, or clouded sensorium is more likely to have delirium rather than dementia.
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