CCRN/PCCN Review Course May 30, 2013

Transcription

1 A & P Review CCRN/PCCN Review Course May 30, 2013 Endocrine Anterior pituitary Growth hormone: long bone growth Thyroid stimulating hormone: growth, thyroid secretion Adrenocorticotropic hormone: growth, adrenal secretion Follicle stimulating hormone/leutenizing hormone: ovulation, testosterone secretion, lactation Kathy Hill, RN, MSN, CCNS Clinical Nurse Specialist Surgical Intensive Care Unit The author has no conflicts of interest to disclose A & P Review Thyroid Posterior pituitary Antidiuretic hormone: water absorption, vasoconstriction Oxytocin: uterine contraction, lactation Thyroxin (T4): made in thyroid, 90% of all hormone Triiodothyronine (T3): converted from T4. Exerts most activity. 99% proteinbound and inactive. Active form is free thyroid Calcitonin: assists Ca++ absorption to bone Parathyroid Parathormone: Ca++, phosphorus regulation

2 A & P Review A & P Review Pancreatic islets Insulin: lowers serum glucose, storage of fat, glycogen, protein synthesis Glucagon: hyperglycemia Somatostatin: inhibits insulin, glucagon, GI motility Adrenal medulla Epinephrine, norepinephrine: sympathomimetic activity Epi: tachycardia, glycogenolysis Norepi: vasoconstriction A & P Review Endocrine Response to Stress: Hypothalamus Adrenal cortex Mineralocorticoids: Na++, K+ regulation via aldosterone Glucocorticoids: protein catabolism, hyperglycemia via cortisol Androgens: precursor to testosterone Acting through the SNS, stimulates adrenal medulla Medulla releases epinephrine, norepinephrine Increase in glucose, fatty acids, heart rate, vasoconstriction, B/P, skeletal muscle metabolism

3 Endocrine Response to Stress: Ant. Pituitary Diabetic Ketoacidosis CRH from hypothalamus stimulates anterior pituitary ACTH release to adrenal cortex Cortisol released Increased fat/protein breakdown, glucose, antiinflammatory effect Decreased (absent) insulin levels Increased counter-regulatory hormones Resembles starvation Diabetic Ketoacidosis Clinical Findings Insidious onset Polyuria Precipitated by missing insulin or increased insulin needs Polydipsia DKA w/coma: Increased mortality Fatigue N/V, abdominal pain

4 Clinical Findings Lab Findings Mental status changes Flushed appearance Fever Kussmaul breathing Glucose WBC Sodium Potassium HCO3 Ketones Metabolic acidosis Lab Findings Anion Gap > 10 or 12 Na (Cl + HCO3) Normal gap = 8-12 Correct fluid/electrolytes Correct acidosis Na = 140 Cl = 98 HCO3 = 20 Education to prevent recurrence

5 Corrected sodium guides fluid replacement NS x 1 liter/hr if Na low ml/kg/hr if Na normal or high D5/NS when BS 200 KPO4 or KCL Correct acidosis with insulin BS q. 1 hr. May take hours to reach BS < 200, bicarb > 15, ph > 7.3 HHNK: hyperglycemic hyperosmolar nonketotic syndrome Education Stress management S & Sx Sick day rules: follow regular meal plan, force fluids, 15 Gm CHO q. 1 hr. End result of uncontrolled hyperglycemia Usually presents without ketoacidosis Insulin levels present, but inadequate

6 Epidemiology Precipitants Usually seen in > 60 Infection, CVA, MI, pancreatitis No Hx of diabetes Mild Type II Mortality rate 10 60% Acute illness Drugs Therapeutic procedures Postop patients with restricted access to water Pathogenesis Clinical Findings Insulin deficiency or lack of effective insulin Marked imbalance in glucose production vs. glucose utilization Diffusion of intracellular fluid to the extracellular space = osmotic diuresis = profound dehydration No ketones No GI symptoms Glucose >1000 Serum osmolality > 380

7 Clinical Findings Hypernatremia Hypokalemia Hypotension Tachycardia Mental status change Fluid/electrolyte replacement Insulin replacement Education. 9NS Usually need more aggressive fluid replacement Watch for overload in elderly

8 Refer to DKA protocol Switch to Education regarding new onset DM Vigilance with oral agents What are living arrangements? Diabetes Insipidus Inadequate ADH (antidiuretic hormone, arginine vasopressin, AVP) 2 types: Central (posterior pituitary) Nephrogenic (renal tubule) Central DI Familial Infectious Neoplasm Trauma Idiopathic

9 Nephrogenic DI Clinical Findings Failure to respond to ADH Hypercalcemia Lithium Intense thirst Dilute urine Hyperactive reflexes Change in mental state Seizures Coma Clinical Findings Hypernatremia Elevated serum osmolality Decreased serum ADH Decreased urine osmolality Decreased specific gravity Decreased urinary sodium U/O 3 20 L/day Fluid replacement with D5W Exogenous ADH replacement for central DI: DDAVP (Desmopressin); aqueous pitressin Chlorpropamide (Diabinese) Thiazides Concentrate urine

10 Education: Fluid replacement with exercise Attention to U/O Avoidance of salt