NR 507 Endocrine System, NR507 Midterm, NR 507 Final

The only way for a hormone to work is through the blood stream. - answer-False. The endocrine cell can also secrete hormones that target cells directly close it. When this occurs, this type of secretion is known as paracrine signaling. Lipid-derived hormones cross the cell membrane and bind to receptors in the cell's cytoplasm - answer-True. This statement is true. Lipid-derived hormones cross the cell membrane and bind to receptors in the cell's cytoplasm. The anterior lobe of the pituitary produces its own hormones - answer-True. This statement is true. The anterior lobe of the pituitary produces its own hormones To be considered a lipid hormone, it must be bound to a protein and it must bind to receptors inside the cell membrane - answer-False. It must be bound to a protein and it bind to receptors on the cell membrane rather than inside the cell membrane. The pineal gland is responsible for regulating the sleep-wake cycle - answer-True. The posterior lobe of the pituitary produces its own hormones - answer-False. The posterior pituitary receives its hormones (oxytocin and ADH) from the hypothalamus. The anterior pituitary produces its own hormones. Aldosterone promotes sodium reabsorption and potassium excretion in the kidneys. - answer-This statement is true. Hyperthyroidism - answer-Elevated Thyroid Hormone Suppressed TSH Enlarged liver Hand tremors Hypothyroidism - answer-Decreased thyroid hormone and Elevated TSH Fatigue Diminished deep tendon reflexes Type 1 DM - answer-Onset 1<10-20 years Associated with diabetic ketoacidosis Symptoms: polyuria, polyphagia, polydipsia Autoimmune:Genetic and environmental factors, resulting in gradual process of autoimmune destruction in genetically susceptible individuals Nonautoimmune:Unknown Strong association with HLA-DQA and HLA-DQB genes acute complications: Diabetic ketoacidosis Type 2 DM - answer-Usually > 40 years of age Associated with hyperosmolar nonketotic coma Symptoms: weakness, weight loss, infections Results from genetic susceptibility (polygenic) combined with environmental determinants and other risk factors Inherited defects in beta-cell mass and function combined with peripheral tissue insulin resistance Associated with long-duration obesity strong genetic association Acute complications: Hyperosmolar nonketotic coma alpha cells - answer-responsible for secreting glucagon beta cells - answer-responsible for secreting insulin and amylin inhibits glucagon secretion delta cells - answer-responsible for secreting gastrin and somatostatin F (PP) Cells - answer-secrete pancreatic polypeptide that stimulates gastric secretions and antagonizes cholecystokinin. Criteria to diagnose Diabetes Type 1 and 2 - answer-FPG ≥126 mg/dL (7.0 mmol/L). Fasting is defined as no caloric intake for at least 8 h* OR 2-h PG ≥200 mg/dL (11.1 mmol/L) during OGTT. The test should be performed as described by the WHO, using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water* OR A1C ≥6.5% (48 mmol/mol). The test should be performed in a laboratory using a method that is NGSP certified and standardized to the DCCT assay* OR In a patient with classic symptoms of hyperglycemia or hyperglycemic crisis, a random plasma glucose ≥200 mg/dL (11.1 mmol/L) *In the absence of unequivocal hyperglycemia, diagnosis requires two abnormal test results from the same sample or in two separate test samples pre-screening for DM - answer-HbA1c (as measured in a DCCT-referenced assay) ≥6.5% OR FPG ≥126 mg/dL (7.0 mmol/L); fasting is defined as no caloric intake for at least 8 hr. OR 2-hr plasma glucose ≥200 mg/dL (11.1 mmol/L) during an OGTT OR In a patient with classic symptoms of hyperglycemia or hyperglycemic crisis, a random plasma glucose ≥200 mg/dL (11.1 mmol/L) Categories of Increased Risk for Diabetes (Prediabetes) - answer-1. FPG 100 to 125 mg/dL 2. 2-hr PG in the range of 140 to 199 mg/dL during an OGTT 3. HbA1c 5.7% to 6.4% Symptoms of hypoglycemia can result from activation of the sympathetic nervous system to cause neurogenic reactions that occur when the blood glucose drops rapidly: - answer-Tachycardia Palpitations Diaphoresis Tremors Pallor Arousal anxiety Other symptoms include: Headache Dizziness Blurred vision Irritability Fatigue Poor judgement Confusion Hunger Seizures Coma Treatment of hypoglycemia - answer-Immediate glucose replacement is required by either oral or intravenous replacement. For patients who are at high risk for developing hypoglycemia, glucagon is prescribed for home use. The practitioner should discuss medications and diet management and proper monitoring of blood glucose levels in the patient education plan. DKA pathophysiology - answer-Insulin deficiency and an increase in counter-regulatory hormones (catecholamines, cortisol, glucagon and growth hormone) are the most significant factors for developing DKA. Under normal circumstances, the counter-regulatory hormones antagonize insulin by increasing glucose production and decreasing use of glucose by the tissues. Extreme insulin deficiency results in decreased uptake of glucose, increased fat mobilization and release of fatty acids and gluconeogenesis, glycogenesis and ketogenesis. Without insulin, the free fatty acids increase the production of ketone bodies in the liver at a high rate that exceeds peripheral use. This causes ketone bodies to accumulate and results in decreased pH and metabolic acidosis. The buffer system is activated in response to metabolic acidosis. Remember that insulin also has an antilipolytic effect. When insulin is deficient, there is increased circulating ketones that contributes to DKA. Also, ketones are normally used by the tissues as an energy source to produce bicarbonate. In DKA, the number of ketones and bicarbonate cannot be balanced. Circulating ketones increase because of impaired use by the peripheral tissues, thus increasing strong acids to freely circulate. Bicarbonate buffering does not occur which leads to metabolic acidosis. Clinical manifestations of DKA - answer-Kussmaul respirations: the individual hyperventilates to compensate for the metabolic acidosis Postural dizziness Central nervous system depression Ketonuria Anorexia, nausea, vomiting Abdominal pain Acetone breath Dehydration Thirst Polyuria Hyperglycemia causes an osmotic diuresis that leads to polyuria along with dehydration. Large amounts of glucose are lost in the urine because the blood glucose is higher than the renal threshold. Electrolyte abnormalities also occur: Hyponatremia Hypophosphatemia Hypomagnesemia The most significant electrolyte disturbance is hypokalemia. The potassium drops because of a shift out of the cell and into the blood caused by the metabolic acidosis. The blood potassium level, though may appear normal The diagnosis of DKA is based on the signs and symptoms described above. The American Diabetes Association's criteria for the diagnosis of DKA include: - answer-Serum glucose level >250 mg/dL Serum bicarbonate level <18 Serum pH <7.30 Presence of an anion gap Presence of urine and serum ketones Treatment of DKA - answer-Treatment is aimed at decreasing the glucose level by administering insulin. Before administering insulin aggressive fluid replacement and correction of potassium must occur. Intravenous fluids are given to correct the potassium level as well as sodium and phosphorous. Throughout treatment, volume status and potassium levels are monitored closely. Once the individual is stable, teaching is provided on the causes of DKA and how to avoid it. Pathophysiology of Hyperosmolar Hyperglycemic Non-Ketoacidosis Syndrome (HHNKS) - answer-HHNKS involves insulin deficiency but it is not as pronounced as the insulin deficiency seen in DKA. Also, the degree of elevated blood glucose and fluid deficit is more pronounced in HHNKS than in DKA. The follow factors contribute to the development of HHNKS: Insulin deficiency Increased levels of counter-regulatory or stress hormones (glucagon, catecholamines, cortisol and growth hormone) Increased gluconeogenesis and glycogenolysis Inadequate use of glucose by peripheral tissues (primarily muscle)-characterized by lack of ketosis Proinflammatory mediators (TNF-α, IL-6, IL-1β) are also involved that also contribute to insulin resistance and hyperglycemia. Less insulin is needed to inhibit fat breakdown needed for effective glucose transport. Therefore, insulin levels are enough to prevent excessive lipolysis but not to use glucose effectively. Clinical manifestations of HHNKS - answer-Patients with HHNKS will have an extremely high glucose level. As a result, there will be glycosuria and polyuria. Because of the amount of glycosuria, the patient is at risk for developing severe volume depletion, increased serum osmolarity, intracellular dehydration and loss of potassium and other electrolytes. Neurological symptoms (stupor and coma) may appear as well and worsen with the degree of hyperosmolarity. Diagnosis of HHNKS - answer-The diagnostic features of HHNKS include: Elevated serum glucose (>600 mg/dL) Near normal serum bicarbonate level and pH Serum osmolarity > 320 mOsm/L Absent or low ketone levels in the urine and serum Treatment of HHNKS - answer-The patient will receive an insulin infusion and fluid replacement. The hypokalemia may be extreme and require several days of infused potassium to return it to a normal level. Sodium and phosphorous replacement may be needed as well. Symptoms of hypoglycemia select all that apply - answer-Symptoms associated with hypoglycemia include pallor, sweating, tachycardia, hunger, restlessness, anxiety, tremors. An individual who presents with Diabetic Ketoacidosis (DKA) will have a blood glucose level of >250 mg/dL. - answer-This statement is true. Metabolic syndrome is characterized by - answer-Metabolic syndrome is characterized by hyperlipidemia, obesity, hypertension. HHNKS is characterized by increased gluconeogenesis and glycogenolysis - answer-true Vitamin D works with parathyroid hormone (PTH) to promote calcium and phosphate absorption in the GI tract and bone - answer-True