EXAM 1 ADV MS

Diabetes Insipidus s/sx, complications, treatmeant, lab values

DISEASE OF THE POSTERIOR PIT. GLAND Cause: hyposecretion of ADH from the posterior pituitary gland and kidneys fail to reabsorb water leading to excessive water loss 3 types of DI: central, nephrogenic, primary DI Central: insufficient secretion of ADH from CNS (caused by brain tumor, surgical removal of pit or hypothalamus, closed head trauma Nephrogenic: Kidneys not responding to ADH even when levels are normal Primary DI: drinking too much water S/sx: HYPER-osmolarity, excess diluted urine, polydipsia, dehydration, decreased skin turgor, fatigue, headache, hypotension Lab values: low urine specific gravity below 1.005 Normal specific gravity 1.010-1.025 low urine osmo <100mOsm/kg Hypernatremia >145 mg/dL High serum osmo >295 mOsm/kg Polyuria 2-20L Treatment: For central DI: Desmopressin (ADH), antidiruetics, IV fluid and hormone replacement (analog to ADH) For nephrogenic DI: low salt diet, thiazide diuretics (sodium and water loss) Nursing consideration: strict I/O's, daily weights, watch for s/sx of hypernatremia (N/V, headache, seizure), monitor specific gravity

SIADH s/sx, complications, treatmeant, lab values

DISEASE OF THE POSTERIOR PIT. GLAND Causes: Too much ADH causing water retention. most common cause is from small cell lung cancer S/sx: hyponatremia, hypo-osmotic, increased GFR, concentrated urine, decreased urine output, fluid overload in lungs, edema Complication: severe hyponatremia causing cerebral edema and irreversible neurological damage Serum Na <115 --> neurological issues and seizures Treatment: fluid restriction if hyponatremia is mild, correct hyponatremia with hypertonic solutions, lasix if there is no hyponatremia, Stadol (ADH inhibitor), Demeclocycline (chronic SIADH), Conivaptan (ADH receptor antagonist) Nursing consideration: seizure precautions, fluid restriction, monitor I/O's, daily weights Lab values: sodium: less than 135 urine osm: greater than 100 blood serum osm: less than 280 specific gravitiy: greater than 1.025

Difference between DKA and HHS

DKA: HYPERGLYCEMIA - can occur in Type 1 and Type 2 but is more common in type 1. - Cause: Physiologic stress or infection - Volume depletion --> HYPOTENSION - Onset: rapid < 24hours - Glucose level >250 - pH 7.35 - Ketone: present - BUN and Creatine increases - Serum Osmolality 300-350 d/t fluid shifting and dehydration HHS: SEVERE HYPERGLYCEMIA - can occur in Type 1 and Type 2 but is more common in type 2. - Cause: Physiologic stress, UTI, found in older adults - Profound volume depletion - Onset: slower - Glucose level >600 - pH: Normal - Ketone: absent - BUN and Creatine increases - Serum Osmolality >350.

DMI vs DMII

DM1: - Body does not make enough insulin d/t absent endogenous insulin - AKA juvenile onset diabetes or insulin dependent - 5-10% of diabetics - 80-90% B cell destruction before s/sx - S/SX: 3 p's and glycosuria (glucose in blood) DM2: - Inadequate amounts of insulin, tissue resistance or overproduction by liver - 90-95% diabetics - risk factors: family genetics, obesity, increasing age, certain ethnic groups - Hyperglycemia may occur without being detected - S/SX: 3p's

Know the different forms of rapid-acting, fast-acting, intermediate and long-acting insulins onset

Doesnt matter when you give the patient long acting insulin Give rapid or short during meal time

HHS s/sx and treatment

s/sx: - Neurological: somnolence, coma, seizures, hemiparesis (one sided weakness), aphasia (loss of ability to express or understand speech) Tx: - LARGE volumes of fluid replacement with NS - Insulin infusion - Monitor signs of FLUID OVERLOAD like pulmonary edema (SOB, increased oxygen demand, dyspnea, orthopnea, anxiety, pink frothy sputum) - monitor cardiac and renal function - electrolyte replacement

hypoglycemia - Know the signs and symptoms and management (when to use PO vs IV vs glucagon to treat low BG)

s/sx: - 3 p's management

Hyperglycemia signs and symptoms and management (when to use PO vs IV vs glucagon to treat low BG)

s/sx: - 3 p's management:

DKA s/sx and treatment

s/sx: - 3 p's hyperglycemia - CORRECT dehydration --> poor skin turgor/dry mucosa, tachycardia, HYPOTENSION - neuro manifestation --> lethary, weakness, confusion - GI --> abd pain, anorexia, vomiting - Respiratory: Kussmaul respiration (rapid deep breathing with pursed kissed lips in response to acidosis, acetone breath Treatment: - Fix dehydration with fluid replacement. Start with NS then when BP is stable, give IVF with dextrose to prevent HYPOglycemia - IV insulin, lower BG SLOWLY to prevent cerebral edema - Electrolyte imbalance and check potassium

Diabetes teaching on Storage of insulin

- Don't share the same vials with patients - Insulin vials and pens can be kept at room temp up to 4 weeks as long as its not below 0 degrees and above 86 degrees. - Avoid sun exposure - Store insulin syringe tip up to prevent clumping at tip - Prefilled combination insulin syringes stable only up to 1 week when stored in the refrigerator (some refilled combo insulins not recommended) -

Know the considerations of diabetes slide

- If exercising, DO NOT inject in the thigh d/t rapid absorption leading to hypoglycemia - Assess insulin administrations barriers like neuropathies or visual/motor deficits - When injecting prefilled insulin syringe, gently roll in palm 10-20x to warm insulin and resuspend particles - alcohol swabs no necessary at home

Hypoglycemic unawareness

- No warning signs/symptoms until glucose level critically low - Related to autonomic neuropathy and lack of counterregulatory hormones - Patients at risk should keep blood glucose levels somewhat higher - Especially seen in long standing DM1 or patients on beta blockers d/t regulated HR - Doesn't happen to newly diagnosed diabetic patients

Diabetes teaching on Administration

- Subcutaneous injection - regular insulin may be given IV - Can't be taken orally - Don't give into a muscle as it is absorbed too rapidly - Absorption is fastest from the abdomen, followed by arm , thigh and buttock - Abdomen is the preferred site - Waste two units to prime the needle - Do not inject in site that will be exercised - Rotate sites - IV insulin given for DKA, post op, or hyperkalemia - Give bolus D50 for hyperkalemia patient with no diabetes first, then IV insulin Watch for hypoglycemia, lipodystrophy, allergic reaction

Thyrotoxicosis/thyroid storm signs and symptoms, complications and treatments

ACUTE and LIFE-THREATENING Patho: uncontrolled hyperthyroidism, caused by too much thyroxine, may progress to the destruction of thyroid tissue leading to hypothyroidism. Can be caused by thyroidectomy d/t release of thyroid hormones in the body Causes: manifested by infection, trauma, surgery S/sx: severe tachycardia --> HF, shock, hypernatremia, seizures, fever, hypertension Treatments: monitor VS, antithyroid medications, propranolol, thyroidectomy for hyperthyroidism

Know how to travel with insulin

Carry the insulin with you!! Notify TSA officer that you have diabetes and are carrying insulin. Insulin pumps and supplies must be accompanied with insulin, and must be clearly labeled. Medical supplies are NOT considered weight Must be labeled with a doctor's note

Pheochromocytoma

Catecholamine-secreting tumor: big tumor in the medulla of adrenal gland, often a single tumor, malignant potential, often idiopathic, associate with genetic conditions Excessive amounts of epinephrine and norepinephrine secreted Classic Triad 1) episodic pounding headache 2) palpitations and tachycardia 3) diaphoresis Treatment: surgical resection

Myxedema signs and symptoms

Cause: severe and long standing hypothyroidism, triggering infection High mortality rate of 40% S/sx: mental sluggish, mask like appearance, skin dull and puffy, periorbital edema, cold intolerant Treatment: thyroid replacing hormone

Know classifications of oral diabetic agents and non-insulin injectables (what's the MOA, when to take it, and major side effects)

Glipizide Meglitinides Biguinides Metformin Glucophage Glucosidase Inhibitors TZDS can be used with and without food, s/e is weight gain and edema Exenatide (Byetta)

What is Dawn phenomenon

Hyperglycemia upon awakening Patho: d/t 2 counterregulatory hormones (growth hormone and cortisol) GH and cortisol oppose insulin causing glucose to rise Affects most diabetics but most severe with adolescence and young adults Check early morning BG to determine if Dawn phenomenon vs Somogyi effect NO HYPOGLYCEMIA IN EARLY MORNING as seen in Somogyi effect Treatment: increase insulin dose or adjust administration time from dinner to before bedtime. Could switch meds to include long acting insulin

What is the Somogyi effect? risk? treatment?

Hypoglycemia early morning (2am-4am) and rebound hyperglycemia upon waking up Patho: Due to too much evening insulin causing counterregulatory hormones (epinephrine, GH, cortisol, glucagon) release which stimulate lipolysis, gluconeogenesis, glycogenolysis --> hypergylcemia Risk: Physician or nurse may give more insulin dose during morning check --> hypoglycemia How to check for suspected Somogyi effect: - patient c/o headache, night sweats, or nightmares upon wakening - check blood sugars 5x a time a day - Reduce insulin in the evening - evening snack

Myxedema coma s/sx and treatments

MEDICAL EMERGENCY: diminished LOC, hypoglycemia, hypoventilation, hypothermia, low hr and bp Causes: severe and long-standing hypothyroidism, triggering infection, sedatives, narcotics, cold S/sx: thinning hair, hypotension, LOC, hypoglycemia, low RR, HR, BP, hyponatremia Treatment: IV thyroid hormone (Levothyroxine), corticosteroids, warming blanket, mechanical ventilation if needed, vasopressors to help with low HR and BP, fluids

Hashimoto's signs and symptoms, complications and treatments

MOST COMMON CAUSE OF HYPOTHYROIDISM Patho: hypothyroidism from autoimmune disease. Body attacks thyroid gland so that no more thyroid hormone (T3 and T4) aren't being produced. Thyroid tissue replaced with lymphocyte and fibrous tissue S/sx: goiter, low T3 and T4, fatigue, intolerance to heat, depressed, constipation, temors in hands Tx: monitor for myxedema coma, life long medication of synthroid or levothyroxine Teaching: - Don't give these patients opiates or sedatives. can lead to myxedema coma - Take Synthroid and Levothyroxine first thing in the morning and 30 mins before breakfast

Hyperparathyroidism - where does PTH exert its effects

Oversecretion of PTH causes calcium reabsorption in the bones and kidneys, increase phosphate secretion, activation of vit D in GI to absorb calcium and phosphorus Causes hypercalcemia and hypophosphatemia

Grave's disease signs and symptoms, complications and treatments

Patho: can be d/t excessive iodine intake, goitrogen-related foods/drugs (inhibit the uptake of iodine causes: hyperthyroidism s/sx: goiter, bulging eyes, exophthalmos d/t impaired venous drainage from orbit and increased fat deposits and fluid in the tissues behind the orbits, weight loss, palpitations, edema in legs Treatment: propanalol for tachycardia, radioactive iodine therapy, thyroidectomy, PTU, Methimazole Complications: thyroid storm, hypothyroidism from radioactive iodine therapy, thyroidectomy, PTU, Methimazole

Cushing's syndrome and disease signs and symptoms, complications and treatments

Patho: excess secretion of corticosteroids from the adrenal cortex or from the administration of glucocorticoids in large doses Cushing's syndrome: Exogenous: chronic use of exogenous corticosteroid (prednisone) Cushing's disease: Endogenous: Cortico-tropic dependent 85% of cushing syndrome is from an ACTH-secreting pituitary adenoma Cortico-tropic independent 15-20% from adrenal tumors and ectopic ACTH-producing tumors from lung or pancreas S/sx: truncal obesity, moon face, buffalo hump, muscle loss/weakness, glucose intolerance, osteoporosis, thin fragile skin, ecchymosis, purple striae on breast/abd/trunk, hair thinning, acne, lowered immune, hyperpigmentation, hirsutism treatment: cortisol tests, ACTH test (high ACTH=r/t hypothalamus/pit, low ACTH and high cortisol=r/t adrenal etiology, ketoconazole, removal of the tumor

Addison's disease

Patho: hyposecretion of adrenal cortex hormones Primary adrenal insufficiency (Addison's disease): deficiency from adrenal cortex, glucocorticoids, mineralocorticoid, and androgen are depressed, 80% or Addison's disease is d/t autoimmune response Secondary adrenal insufficiency: lack of pituitary ACTH secretion from pituitary disease, exogenous corticosteroids S/sx: slow onset (90% of cortex is destroyed before symptoms occurs) weakness, anorexia, weightloss, nausea, abd pain, skin hyperpigmentation, joint pain, HYPOTENSION Treatment: requires lifelong replacement of glucocorticoids

Hypoparathyroidism signs and symptoms, complications and treatments

Patho: rare and can be d/t accidental removel of parathyroid gland or severe hypomagnesemia Causes: hypocalcemia and hyperphospatemia S/sx: numbness and tingling in the face, positive Chvostek and Trousseau's sign, tetany Complications: cardiac dysrhythmias, hypotension, seizure precaution Treatment: Slow IV calcium gluconate for tetany, oral calcium supplements/foods, low phos diet, phosphate binders

Facial feature of acromegaly (refer to slide)

Patho: rare d/t benign autonomic GH secreting pituitary adenoma FACIAL FEATURES: - Mandibular over growth (mandibular prognathism) - Widened/thickened nose - prominant cheekbones - forehead buldge (frontal bossing) - Jaw malocclusion - Enlarged tongue - enlarged facial bones - Large hands and feet Complications: - Hypertension - atherosclerosis - cardiomegaly - Increased mortality d/t cardiac hypertrophy - DM2 - arthritis/joint pain - headache/seizures

Competencies of QSEN

Patient-centered care Evidence-based practice Teamwork and collaboration Safety Quality improvement Informatics

Primary vs secondary vs tertiary hyperparathyroidism

Primary: Most common d/t parathyroid tumor and long-term lithium use Secondary: hypocalcemia caused by chronic renal failure (reabsorbs calcium and excretes phosphorus --> overworks the parathyroid), intestinal malabsorption, hyperphosphatemia, Vit D deficiency Tertiary: hyperplasia of the parathyroid gland, seen in patients with new kidneys after long-standing dialysis

Primary vs secondary hyperthyroidism

Primary: decreased TSH and increased thyroxine Secondary: increased TSH and increased thyroxine

metabolic syndrome

Risk factors that increases an individual's chance of developing HTN, cardiovascular disease, stroke and diabetes Etiology: insulin resistance related to excessive visceral fat - 1 in 3 adults of metabolic syndrome - DX: when 3 or more of the following are present 1. Waist circumference >40 men, >35 female 2. Triglyceride >150mg/dl or current treatment 3. HDL <40 men, <50 women or tx for low HDL 4. BP >130 SBP >85 DBP, or treatment for high BP 5. FGB >110mg/dL or treatment for high BG

Hypoparathyroidism - signs and symptoms of hypocalcemia

S/sx of hypocalcemia: Chvostek and Trousseau's sign Muscle cramps tingling of lips, fingertips, feet Hyperreflexia Hypotension Cardiac dysrhythmia

Hyperparathyroidism: signs and symptoms, complications and treatments

STONES, GROANS, BONES, THRONES Patho: hypersecretion of PTH by parathyroid gland S/sx: hypercalcemia, hypophosphatemia, fatigue/muscle weakness, skeletal pain/tenderness, bone deformities/fractures, anorexia/weightloss, constipation Complications: osteoporosis, pathologic fractures, constipation, kidney stones, cardiac dysrhythmias Treatments: parathyroidectomy, Alendronate (Biphosphate) to prevent bone resorption, routine labs

Blood sodium levels, blood serum osmolality levels, urine osmolality levels, specific gravity

Sodium: 135-145 Blood serum osm : 280-295 Urine osm: low >100, high <100 Specific gravity: 1.010-1.025

Trans-sphenoidal hypophysectomy: Indication for the procedure, Nursing care and teaching, post op care, Complications

Surgeon uses an endoscope into the nose to remove the pituitary gland and remove the tumor Indication: hyperpituitarism Nursing care/teaching: - avoid vigorous coughing, straining, and sneezing to prevent CSF leakage - Need for lifelong hormone replacement therapy after total hypophysectomy - decrease or loss of fertility Post-op care: - monitor VS for neuro changes (look for signs of hematoma) HOB 30 degrees to avoid pressure on the Sela Tursica to reduce headaches - Gentle mouth care Q4hrs, no tooth brushing for 10 days so suture line stays intact, avoid coughing - check for any clear nasal drainage (CSF leak) --> Glucose >30mg/dL indicates CSF - Transient cerebral edema or DI common loss of ADH --> treat with IV vasopressin Complications: epitaxis, cerebral edema, DI and CSF leak

what does cortisol regulate

arousal, cognition, mood, sleep, metabolism, cardiovascular tone, and growth and reproduction

Draw up insulin

clear to cloudy

What does ADH regulate?

water excretion from kidney (osmolality of body)