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Sulfonylureas (most commonly prescribed for diabetes) |
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↑ Insulin production from pancreas ↓ Chance of prolonged hypoglycemia 10% experience decreased effectiveness after prolonged use Examples Glipizide (Glucotrol) Glimepiride (Amaryl) |
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Increase insulin production from pancreas Taken 30 minutes before each meal up to time of meal Should not be taken if meal skipped Examples Repaglinide (Prandin) Nateglinide (Starlix) |
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Reduce glucose production by liver Enhance insulin sensitivity at tissues Improve glucose transport into cells Do not promote weight gain Example Metformin (Glucophage) |
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Promotes glucose transport from bloodstream across cell membrane to cytoplasm of cell Decreases glucose in the bloodstream |
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The tendency of the body to react to extremely low blood sugar (hypoglycemia) by overcompensating, resulting in high blood sugar. |
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When we sleep, hormones are released to help maintain and restore cells within our bodies. These counterregulatory hormones (growth hormone, cortisol and catecholamines) cause the glucose level to rise. For people with diabetes who do not have enough circulating insulin to keep this increase of glucose under control, the end result is a high glucose reading in the morning. |
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Balance Regular meals Five portions of fruit/vegetables Spread fruit throughout the day |
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Term used to describe rise in blood glucose levels after consuming carbohydrate-containing food |
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Confusion, diaphoresis, hunger, visual disturbances, irritability May be confused with intoxication or mental illness Seizures, coma and death |
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common manifestations of diabetes |
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Diabetic Ketoacidosis (DKA) |
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Definition
Blood glucose ≥ 250 mg/dL Ketosis Ketonuria/ketonemia Metabolic acidosis ↓pH, PCO2, HCO3 Dehydration Electrolyte imbalances ↓ Na, ↓/↑K, Cl, PO4 |
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Hyperosmolar hyperglycemic non-ketotic syndrome |
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Definition
Blood glucose ≥ 600 mg/dL Dry mouth Extreme thirst Raised temperature over 101F More common in type II diabetes |
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Excessive thirst Blurred vision Weakness Headache Acetone breath *Kussmaul respirations Deep, non-labored, rapid Orthostatic hypotension Weak, rapid pulse Dehydration* GI symptoms Anorexia, N & V, *vomiting & abdominal pain |
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disorders of the blood vessels Large vessels (macrovascular) – Heart Dz, stroke Greater frequency and earlier onset for those with Diabetes |
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Accelerates the development of HTN |
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Sensory Paresthesias of the hands &/or feet Autonomic Gastroparesis, bowel incontinence, & diarrhea, heart burn, constipation Urinary retention Sexual dysfunction Decrease in vaginal lubrication, libido Silent MI |
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results from excess secretion of growth hormone (GH), very rare Bone and soft tissue overgrowth (bones increase in thickness and width but not length) Manifestations: Enlargement of hands/feet Thickening/enlargement of face/head Sleep apnea Signs of: DM , Cardiomegaly, HTN Treatment: Returning GH levels to normal Surgery Radiation Drug Therapy Combination |
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rare, decrease in one or more of the pituitary hormones: The anterior pituitary gland secretes: adrenocorticotrophic hormone (ACTH) thyroid-stimulating hormone (TSH) follicle-stimulating hormone (FSH) luteinizing hormone (LH), GH prolactin The posterior pituitary gland secretes: ADH Oxytocin
Most deficiencies involve GH and gonadotropins (e.g., LH, FSH) due to a pituitary tumor |
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results from an overproduction or oversecretion of ADH fluid retention serum hypoosmolality dilutional hyponatremia Hypochloremia concentrated urine in presence of normal or increased intravascular volume normal renal function Most common cause - lung cancer Treatment directed at underlying cause goal to restore normal fluid volume and osmolality Fluid restriction results in gradual, daily weight reductions, progressive rise in serum sodium concentration and osmolality, and symptomatic improvement |
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defciency of production or secretion of ADH or decreased renal response to ADH causing fluid and electrolyte imbalances due to increased urinary output and increased plasma osmolality -May be transient or chronic |
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Thyroid gland hyperactivity with sustained increase in synthesis and release of thyroid hormones |
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autoimmune disease marked by thyroid enlargement and excessive thyroid hormone secretion classic finding - exophthalmos, a protrusion of eyeballs from the orbits Treatment antithyroid medications radioactive iodine therapy subtotal thyroidectomy – causes hypothyroidism (on replacement thyroid hormone medication for life) |
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(related to destruction of thyroid tissue or defective hormone synthesis) |
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(related to pituitary disease with decreased TSH secretion or hypothalamic dysfunction with decreased thyrotropin-releasing hormone [TRH] secretion) |
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related to thyroiditis or from a discontinuation of thyroid hormone therapy |
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Manifestations: fatigue, lethargy, personality and mental changes, decreased cardiac output, anemia, and constipation. myxedema, an accumulation of hydrophilic mucopolysaccharides in dermis and other tissues. This mucinous edema causes characteristic facies of hypothyroidism (i.e., puffiness, periorbital edema, and masklike affect) Treatment : Restoration of euthyroid state as safely and rapidly as possible with hormone replacement therapy Levothyroxine (Synthroid) drug of choice |
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Increased secretion of parathyroid hormone (PTH) - leads to hypercalcemia and hypophosphatemia Manifestations: weakness, loss of appetite, constipation, emotional disorders, and shortened attention span Major signs: Osteoporosis, fractures, and kidney stones Neuromuscular abnormalities: muscle weakness in proximal muscles of lower extremities |
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Rare, results from inadequate circulating PTH resulting in hypocalcemia Most common cause is iatrogenic accidental removal of parathyroid glands or damage to these glands during neck surgery Manifestations Tetany - tingling of lips, fingertips, ncreased muscle tension with paresthesias and stiffness Painful tonic spasms of smooth and skeletal muscles (extremities and face) Laryngospasms Positive Chvostek/Trousseau sign are usually present |
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Cushing Syndrome (dysfunction of adrenal cortex) |
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Caused by excessive corticosteroids, particularly glucocorticoids Most common cause - iatrogenic administration of exogenous corticosteroids (e.g., prednisone) Manifestations: centripedal or generalized obesity, “moon facies” (fullness of face), purplish red striae below the skin surface, hirsutism in women, hypertension, and unexplained hypokalemia Treatment: Surgery Drug therapy |
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Addison's Disease (adreno-cortical insufficiency) |
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all three classes of adrenal corticosteroids (glucocorticoids, mineralocorticoids, and androgens) are reduced – usually autoimmune Manifestations: Slow onset: weakness, weight loss, anorexia Skin hyperpigmentation in sun-exposed areas of body, at pressure points, over joints, in palmar creases Treatment : Replacement therapy (Hydrocortisone most commonly used) has both glucocorticoid and mineralocorticoid properties During times of stress, dosage is increased to prevent addisonian crisis |
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Characterized by excessive aldosterone secretion commonly caused by small solitary adrenocortical adenoma Main effects: Sodium retention and potassium and hydrogen ion excretion Key sign of this disease: hypertension with hypokalemic alkalosis Treatment: Mostly surgical removal of adenoma (adrenalectomy) Patients with bilateral adrenal hyperplasia are treated with drugs. Calcium channel blockers may be used to control BP Patients are taught to monitor own BP and need for monitoring |
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Pheochromocytoma (Disorders of the adrenal medulla) |
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Rare, characterized by an adrenal mostly benign medulla tumor that produces excessive catecholamines (epinephrine, norepinephrine) Secretion of excessive catecholamines results in severe HTN Undiagnosed and untreated, may lead to diabetes mellitus, cardiomyopathy, and death Manifestations: severe, episodic hypertension accompanied by classic triad of (1) severe, pounding headache, (2) tachycardia with palpitations and profuse sweating, and (3) unexplained abdominal or chest pain Attacks may be provoked by many medications, including antihypertensives, opioids, radiologic contrast media, and tricyclic antidepressants Treatment: Surgical removal of tumor |
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onset: 30 minutes to 1 hour peak: 2-3 hours duration: 3-6 hours |
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Intermediate/NPH/Cloudy/Lente |
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onset: 2-4 hours Peak: 4-10 hours Duration: 10-16 hours |
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long-acting/ultralente (cloudy) |
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onset: 1-2 hours Peak: no pronounced peak Duration: 24+ hours |
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c. It interacts with plasma membrane receptors to produce enzymatic actions that affect protein, fat, and carbohydrate metabolism.\ |
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a. phentolamine (Regitine). |
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A female client with a history of pheochromocytoma is admitted to the hospital in an acute hypertensive crisis. To reverse hypertensive crisis caused by pheochromocytoma, nurse Lyka expects to administer: |
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Rapid-acting: lispro, aspart, glulisine |
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Onset: 15 minutes Peak: 60-90 minutes Duration: 3-4 hours |
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