Exam #4: Ch. 17, 48-50 (Endocrine System)

Ch. 17-Fluid and Electrolytes
1. Review calcium regulation.
-present in the body as free or ionized, bound to proteins like albumin, and complexed with phosphate, citrate, or carbonate
-serum calcium levels reflect all three forms
*plasma acidosis: decreases albumin bound calcium, thus increasing ionized calcium
*plasma alkalosis: increases albumin bound calcium, thus decreasing ionized calcium
*calcium balance controlled by parathyroid hormone (PTH), calcitonin, and vitamin D
-PTH: produced by parathyroid gland and stimulated by low serum calcium
>increases movement of calcium out of bones, GI absorption of calcium, and renal tubule reabsorption of calcium
-calcitonin: produced by thyroid gland and stimulated by high serum calcium
>opposes PTH action—decreases GI absorption, increases calcium deposition into bone, and promote renal excretion
-vitamin D: formed through UV rays in precursors found in skin or diet
>aids in absorption of calcium in GI

2. Identify clients at risk for calcium imbalance.
*hypercalcemia
-hyperparathyroidism
-malignancies: cause bone destruction from tumor invasion or secrete a parathyroid-like protein to stimulate calcium release from bones
-vitamin D overdose
-prolonged immobility: bone mineral loss and increased plasma calcium concentration
-rarely occurs from increased calcium intake
*hypocalcemia
-removal or injury of parathyroid gland
-acute pancreatitis: causes lipolysis which produces fatty acids that combine with calcium ions
-multiple blood transfusions: citrate used as anticoagulant binds to calcium
-low calcium diet or decreased absorption from laxative abuse or other syndromes

3. Recognize the signs and symptoms of hypercalcemia and hypocalcemia.
*hypercalcemia
-reduced excitability of muscles and nerves: decrease in memory, confusion, disorientation, fatigue, muscle weakness, constipation, cardiac dysrhythmias, and renal calculi
*hypocalcemia
-increased excitability of muscles and nerves: tetany, manifested by Chvostek’s sign and Trousseau’s sign, laryngeal stridor, dysphasia, numbness and tingling around the mouth or in extremities, and ventricular tachycardia from decreased cardiac contractility

4. Use the NP to provide care to a client with a calcium imbalance.
*assessment
-subjective: ALOC, confusion, memory loss, fatigue, muscle weakness, numbness and tingling around mouth and extremities
-objective: disorientation, constipation, cardiac dysrhythmias, renal calculi, tetany, dysphasia, laryngeal stridor
-dx: serum calcium levels, ionized calcium levels

*diagnoses
-risk for injury

**planning/implementation
*hypercalcemia
-promote excretion of calcium in urine: loop diuretics, hydrate with isotonic saline solutions, 3000-4000 ml fluid intake (also to decrease kidney stone formation)
-lower serum calcium levels: synthetic calcitonin, low calcium diet
-enhance bone mineralization: mobilization with weight-bearing activity
-Aredia: hypercalcemia associated with malignancy; inhibits osteoclast action which breaks down bone and releases calcium as a result
-Mithracin: cytotoxic antibiotic; inhibits bone resorption to lower serum calcium levels
*hypocalcemia: treat the underlying cause
-oral or IV calcium, but not IM
-high calcium diet with vitamin D supplements or calcium supplements for low tolerance of dairy products
-treat pain and anxiety to prevent respiratory alkalosis induced hypocalcemia

Ch. 48-Nursing Assessment: Endocrine System
1. Review the normal regulation of hormonal secretion.
-stimulate or inhibit hormone synthesis or secretion using:
*simple feedback: based on blood levels of a particular substance
-negative feedback: increase or decrease of secretion depending
>calcium regulation: low serum calcium stimulates PTH to increase calcium levels, once achieved the increased calcium levels inhibit further PTH release
-positive feedback: increases target organ action beyond normal
>pressure receptors in the vagina during birth stimulate more oxytocin secretion to make stronger uterine contractions
*complex feedback: hormone stimulation or inhibition involving multiple glands
*nervous system control: hormone secretion directly affected by nervous system actvity like pain, emotion, sexual excitement, and stress
*physiologic rhythms: secretions by rhythms originating in the brain structure like the circadian rhythm related to sleep-wake or dark-light cycles

2. Review the actions of the different hormones and their sources.
**hypothalamus: secretes releasing and inhibiting hormones to the anterior pituitary gland to stimulate or inhibit release of hormones
*releasing hormone:
-corticotropin-releasing hormone (CRH)
-thyrotropin-releasing hormone (TRH)
-growth hormone-releasing factor or somatotropin-releasing hormone
-gonadotropin-releasing hormone (GnRH)
-prolactin-releasing hormone
*inhibiting hormone
-somatostatin: inhibits growth hormone release
-prolactin-inhibiting hormone
**anterior pituitary
*tropic hormone: precursor hormones with control the secretion of hormones by other glands
>thyroid stimulating hormone (TSH), adrenocortiocotropic hormone (ACTH), follicle stimulating hormone (FSH), and luteinizing hormone
*growth hormone: affects growth and development of skeletal muscle and long bones
*prolactin: stimulates breast development for lactation after childbirth
**posterior pituitary: hormones actually produced in hypothalamus, but stored here until release is triggered
*antidiuretic hormone (ADH): regulates fluid volume by stimulating reabsorption of water in renal tubules, making concentrated urine; also a potent vasoconstrictor
*oxytocin: stimulates ejection of milk into mammary glands and contraction of uterine smooth muscle
**thyroid gland: regulated by TSH from anterior pituitary
*thyroxine (T4) and triiodothyronine (T3): affect metabolic rate, caloric requirements, oxygen consumption, carbohydrate and lipid metabolism, growth and development, brain functions, and other nervous system activities
*calcitonin: lowers serum calcium levels by inhibiting calcium resorption from bone, increasing calcium storage in bones, and increasing kidney excretion of calcium and phosphorus
**parathyroid glands
*parathyroid hormone (PTH): regulate blood level of calcium
-stimulates bone resorption and inhibits bone formation
-increases calcuim reabsorption and phosphate excretion
-stimulates conversion of vitamin D in most active form to enhance intestinal absorption of calcium
**adrenal glands
*adrenal medulla
-catecholamines: stress response neurotransmitters
*adrenal cortex: any hormones secreted are referred to as corticosteroids except androgens
-cortisol: glucocorticoid; regulates blood glucose concentration by stimulating hepatic conversion of amino acids to glucose; necessary to maintain life
>antiinflammatory action, maintains vascular integrity and fluid volume
-aldosterone: mineralocorticoid; maintain extracellular fluid volume by promoting reabsorption of sodium and excretion of potassium and hydrogen ions
-adrenal androgens: stimulates pubic and axillary hair growth and sexual drive in females in the form of estrogen
>negligible amounts in men
**pancreas (islets of Langerhans)
*glucagon: increases blood glucose through stimulation of glycogenolysis, gluconeogenesis, and ketogenesis
*insulin: facilitates glucose transport into cell membrane

3. Effects of the sympathetic and parasympathetic system.
-insulin secreted by both systems

Ch. 49-Nursing Management: Diabetes Mellitus
1. Differentiate the pathophysiology of the different types of DM.
-Type 1 DM: destruction of islets by immune system, therefore there is a little to no insulin production
-Type 2 DM: pancreas can produce insulin, but is insufficient and/or poorly utilized by the body
-Gestational: high blood glucose during pregnancy and high risk of developing type 2 diabetes
-Pre-Diabetic: not enough to be diagnosed, but high risk of type 2 diabetes if not treated
>Fasting glucose and OGTT higher than normal
-Secondary Diabetes: result of another medical condition or treatment which causes high glucose levels

2. Differentiate normal, pre-diabetic, and diabetic blood-glucose levels.
-normal: 70-120 mg/dl
-pre-diabetic: >100 -<126>140-<200 mg/dl casual
-diabetic: >126 mg/dl when fasting or >200 mg/dl casual

3. Use the NP to provide care to a pre-diabetic patient and a diabetic patient.
*assessment
-subjective: obesity, family history, history of viral infections, surgery, or medical conditions, thirst, hunger, poor healing
-objective: Kussmaul respirations (rapid, deep breathing with fruity odor), weight loss
-dx: Hb A1c, FSBG, IGT, IFG

*diagnoses
-ineffective theraupeutic regimen management
-risk for injury
-risk for infection
-powerlessness
-imbalanced nutrition: more than body requirements

*planning
-active patient participation
-few or no episodes of acute hyperglycemic emergencies or hypoglycemia
-maintain blood glucose within normal range
-prevent/delay chronic conditions
-maintain ADLs with minimal stress

*implementation
-identify those at risk
-teach how to monitor blood glucose regularly
-teach insulin therapy
-emphasize personal hygiene and foot care
-medical alert bracelet and ID

4. Know the action of the oral hypoglycemic agents.
*not insulin, works to improve mechanisms which insulin and glucose are produced and used
*three main actions: increases insulin production from pancreas, decreases glucose production from liver, and/or improves insulin use by body
-sulfonylureas (Glucotrol, Amaryl): increases insulin production from pancreas
-meglitinides (Prandin, Starlix): increases insulin production from pancreas
-biguanides (Glucophage): decreases glucose production from liver, improves insulin use by body
-alpha-glucosidase inhibitors (Precose): slows absorption of carbohydrates in small intestine
-thiazolidinediones (Actos, Avandia): greatly improves insulin use by body

5. Know the onset, peak action, and duration of the different types of insulin.
*rapid-acting (Humalog, Novolog, Apidra, Exubera): peaks 60-90 minutes
-onset: 15 minutes
-duration: 3-4 hours
*short-acting (regular): peaks 2-3 hours
-onset: 30-60 minutes
-duration: 3-6 hours
*intermediate-acting (NPH): peaks 4-10 hours
-onset: 2-4 hours
-duration: 10-16 hours
*long-acting (Lantus, Levemir): no peak
-onset: 1-2 hours
-duration: 24+ hours

6. Explain the information needed to teach a diabetic patient about exercise and the management of their diabetes.
-teach patient it is essential to diabetes management because it increases insulin receptor sites, lowers blood glucose, and contributes to weight loss
-individualized exercise plan: done after medical clearance with a gradual progression
-monitor blood glucose before, during, and after
-exercise after meals with small carbohydrate snacks every 30 minutes

7. Explain the pathophysiology of DKA, HHS, hypoglycemia and hyperglycemia.
*DKA: profound deficiency of insulin causes breakdown of fat with ketones as a byproduct
-lowers pH causing metabolic acidosis
-ketones are excreted in the urine and electrolytes become depleted
*HHS: inadequate hydration paired with polyuria cause blood glucose to be >400 mg/dl and high serum osmolality
*hypoglycemia: too much insulin in proportion to glucose in the blood
*hyperglycemia: too much glucose in proportion to insulin in the blood

8. Use the NP to provide care for a patient with DKA, HHS, and hypoglycemia
**DKA
*assessment:
-subjective: type 1 diabetes, illness or infection, poor self management, neglect, lethargy, weakness, nausea, vomiting
-objective: inadequate insulin dosage, dehydration, abdominal pain, Kausmall respirations (rapid, deep rhythm), fruity smelling breath
-dx: blood glucose >300 mg/dl, ABG pH <7.3,>add D5 to prevent hypoglycemia when blood glucose levels approach 250 mg/dl
>replace potassium
>sodium bicarbonate, if pH <7>400 mg/dl, increased serum osmolality, and little to no ketone bodies in blood or urine (unlike DKA because of circulating insulin)

*diagnoses:
-risk for injury

*planning (like DKA):
-maintain patent airway
-correct fluid/electrolyte imbalance, more than DKA
-insulin therapy (after fluids have begun)

*implementation:
-administer oxygen
-1/2 NS or NS to restore urine output and blood pressure
>add D5 to prevent hypoglycemia when blood glucose levels approach 250 mg/dl
>replace potassium
>sodium bicarbonate, if pH <7>70 mg/dl, investigate further; begin treatment if <70 mg/dl
--alert patients should be given 15-20 g of a simple carbohydrate like orange juice
--avoid fatty foods as they decrease absorption of sugar
--continue to monitor BG and give scheduled snacks
-if after 2-3 doses of simple carbohydrates do not work or the patient is not alert
--administer 1 mg of glucagon IM or SQ
--give complex carbohydrate after recovery
--20-30 ml D50 IVP in acute care setting

9. List and explain the chronic complications resulting from diabetes.
*microvascular angiopathy: thickening of capillary and arteriole vessel membranes particularly in the eyes, kidneys and skin
-retinopathy:
--proliferative: most severe; occlusion of small blood vessels involving retina and vitreous
--non-proliferative: most common; partial occlusion of small blood vessels in retina
-neuropathy: damage of vessels which supply blood to glomeruli of kidneys; nerve damage caused by metabolic complications of diabetes
--sensory: abnormal sensation of hands and/or feet bilaterally
--autonomic: can affect nearly all body systems
-integumentary problems: infection and necrosis caused by a combination of loss of nerve sensation and poor blood circulation

10. Use the NP to provide care to a patient specific to each of these complications.
*angiopathy:
*retinopathy: treat early with annual dilated eye exams
-photocoagulation
-cryotherapy
-vitrectomy
*neuropathy: tight glucose control, BP management, yearly screening of microalbuminuria in urine and serum creatinine, drug therapy
*integumentary problems: treat infections quickly and vigorously

Ch. 50-Nursing Management: Endocrine Problems (incomplete)
2. Differentiate between the signs and symptoms of Addison's disease and Cushing's disease.
-Addison's disease: lack of corticosteroids; progressive weakness, fatigue, weight loss, skin hyperpigmentation, anorexia, confusion
-Cushing's disease: excess corticosteroids; weight gain (moon face, trunk weight, water retention), secondary diabetes, purple-red straie, slow wound healing,