Nursing Exam Review: Acromegaly, Acute Glomerulonephritis, Acute Renal Failure, Addisonian Crisis, Burn Center Referral, Exams of Nursing

Download Nursing Exam Review: Acromegaly, Acute Glomerulonephritis, Acute Renal Failure, Addisonian Crisis, Burn Center Referral and more Exams Nursing in PDF only on Docsity! NURS 470 EXAM 2 Acromegaly - ANSToo much GH Onset in adulthood After epiphyseal growth Symptoms: bones get wider, big feet, big hands, large jaw, growth of bones and soft tissues Diagnostics: history, physical assessment, CT, MRI, Evaluation of plasma IGF-1 levels (insulin-like growth factors): Stimulates growth of bones and soft tissues - more reliable measure than GH levels because GH normally fluctuates Oral glucose challenge: GH concentration falls during oral glucose tolerance test. In acromegaly, GH levels do not fall below 1 ng/mL Treatment: focuses on returning GH levels to normal through surgery (tumor removal), radiation, and drug therapy Octreotide acetate (sandostatin): common treatment for acromegaly. Most common side effects are diarrhea, nausea, gallstone formation, and abdominal discomfort. Prognosis depends on age of onset and when the treatment is initiated, and tumor size Acute glomerulonephritis - ANSCaused by infections, immune diseases, vasculitis, HTN, diabetic neuropathy Acute post-streptococcal glomerulonephritis and rapidly progressive glomerulonephritis are examples of acute incidences and symptoms are based on cause Goodpasture syndrome: autoimmune disease in which there are circulating antibodies to the glomerular basement membrane. Treatments include corticosteroids, immunosuppressive drugs, plasmapharesis, and dialysis Acute renal failure - ANSAKA acute kidney injury Partial or incomplete impairment of kidney function Abrupt decrease in kidney function Results in an inability to excrete metabolic waste products and water from the body Has a rapid onset and ranges from a slight deterioration in kidney function to severe impairment. Is potentially reversible but is one of the leading causes of inpatient mortality Occurs in 5-30% of hospitalized patients Most commonly occurs following severe prolonged hypotension, hypovolemia, or exposure to nephrotoxic agents Sudden increased in BUN and Cr Urine output <40 mL/hr These changes can take place over hours to days, are typically associated with a decrease in cardiac output, and can often be reversible if treated early. There are no kidney biomarkers or tests to detect early kidney injury so the time of injury and time of detection/treatment can be detrimental One of the earliest signs of ARF is intake and output Acute tubular necrosis - ANSMost common intrarenal cause of ARF. It is the necrosis of the renal tubule tissue. ATN is associated with tissue destruction, leading to a high incidence of permanent renal damage Damage to renal tubular epithelium due to: 1. Ischemic injury: Decreased perfusion - decreased CO, volume loss, severe hypotension Shock: hypovolemic, cardiogenic, septic Sepsis & anaphylaxis 2. Nephrotoxic injury: Endogenous - rhabdo, TLS Antimicrobials: cephalosporins, antifungals, antivirals Immunosuppressants Chemotherapy NSAIDs Street drugs: heroin, amphetamines, PCP Nephrotoxicity risk can be reduced by keeping the patient well hydrated before and during treatment and keeping the patient's hemodynamic status stable Addisonian crisis - ANSEmergent condition - acute adrenal insufficiency ICU monitoring Causes: stress, pregnancy, surgery, infection, dehydration, anorexia, fever, emotional upheaval Lack/insufficient hormone replacement. Body cannot produce enough cortisol to deal with the stress Lack of aldosterone will lead to hypotension, hyponatremia, and hypokalemia. Clinical manifestations: penetrating pain in back, depressed or changed mentation, volume depletion, hypotension, loss of consciousness, shock Addisonian crisis management - ANSCorrect fluid and electrolyte imbalances - rapid rehydration with NS Replace steroids: hydrocortisone 100 mg IV, followed by 100 mg q 8 hr x 24 hr then PO hydrocortisone Correct hypoglycemia: D5W Feeling dizzy when standing up Loss of appetite, nausea, vomiting, confusion, restlessness, sleepiness Flank pain Increased BUN/Cr Also can have decreased immunity and susceptibility to infection, itching, platelet dysfunction (bruising, petechiae) Encephalopathy due to buildup of uremic toxins in the brain. Impaired wound healing, pericarditis due to accumulation of uremic toxins, and increased gastric acid production leading to GI complications. ARF interventions - ANSPrevention: avoid nephrotoxic drugs: NSAIDs and ACE inhibitors. Avoid IV contrast dye in high risk patients Monitor for effects of altered protein binding sites. Monitor for altered absorption, distribution, and metabolism: drug toxicity. Isotonic solutions for hypervolemia PRBCs and isotonic NS for hypovolemia due to blood loss Glucocorticoids for inflammation High calorie, low protein diet to maintain nutritional status Pharm: diuretics, electrolyte replacement, administration of EPO if needed Non-pharm: fluid restriction, frequent urination, diet low in K, low in Na, and protein ARF labs - ANSIncreased BUN Increased Cr Hyperkalemia: damaged tubule unable to exchange K for Na or H Hyponatremia: due to overhydration leading to dilution in serum Metabolic acidosis: H ion secretion and bicarbonate ion production diminish. Lungs cannot fully compensate Hyperphosphatemia/hypocalcemia Anemia *Creatinine is the most reliable/sensitive indicator of renal health. Daily weight is best indicator of fluid status, and earliest sign of renal failure is 24 hr I/O* Urinalysis: RBCs, WBCs, specific gravity and osmolality - representing tubular damage ABG: injured kidneys unable to remove excess hydrogen ions and production and absorption of bicarb is reduced, resulting in metabolic acidosis ARF patho - ANSInteraction of tubular and vascular events result in ARF Primary cause of ATN is ischemia. Ischemia, activation of RAAS, and tubular obstruction by cellular debris result in significant reduction of GFR. As nephrotoxins damage the tubular cells, these cells are lost through necrosis, and the tubules become more permeable. This results in filtrate absorption and a reduction in the nephrons ability to eliminate waste Assessment of the endocrine system - ANSNursing process Focuses on the manifestations of the hormone excess or deficiency or metabolic dysfunction Collect thorough history: present/past/surgical/meds/allergies Chief complaint/general appearance/vitals/assessment When problem began: onset, duration, pain, clinical manifestations, review of systems Burn center referral - ANSBurn center characterstics: Hospital based Institutional commitment to burn care Medical professionals with burn care expertise Acute and rehab services Provides educational programs Participates in burn care research Defined physical location Specialized nursing care unit Referral criteria: 2nd degree burns >10% TBSA Burns to face, hands, genitalia, feet, perineum, and major joints 3rd degree burns Electrical injury (lightning included) Chemical burns Inhalation injuries Burns accompanies by pre-existing medical conditions Burns accompanied by trauma, where burn injury poses greatest risk of morbidity and mortality Burns to children in hospitals without pediatric services Patients with special social, emotional, or rehabilitative needs Burn depth - ANSFactors: Temperature Duration of contact Dermal thickness Blood supply If the skin hurts, we know that it is alive so that is a good thing. If it does not hurt, the skin is dead Special consideration: very young or elderly patients have thinner skin Burns primary survey - ANSAirway: chin lift, jaw thrust, insert OPA, assess need for intubation. Maintain inline cervical immobilization for patients that may have trauma Breathing: verify breath sounds and assess rate and depth. Monitor chest wall for excursion if there are deep torso burns because that skin can turn to leather and get compartment syndrome. Administer high flow O2. CO sticks to hemoglobin and does not let go, so have to give 100% oxygen until carboxyhemoglobin levels are less than 15% Circulation: monitor BP, pulse, skin color. Establish IV access - may have to cut open the skin. Have to monitor for compartment syndrome for at least 72 hours (skin color, pulses). If there is a circumferentially burned extremity, at risk for compartment syndrome Disability: neurological deficit. If not alert and oriented, consider associated injuries, CO poisoning, substance abuse, hypoxia, or pre-existing medical condition. Can use AVPU rating system: Alert; Responds to verbal stimuli, Responds to painful stimuli only; Unresponsive Exposure: remove all clothing and jewelry. Maintain patient's temperature - do not put ice on a burn. Keep warm, in a dry sheet, and use warm IV fluids Care of patient with anemia - ANSMonitor oxygenation, cardiac, pulmonary, vascular, neuro, integumentary, GI, and lab results. Investigate possible reasons for anemia through H&P Administer related drug therapy and monitor for effects (oxygen, EPO, nutritional supplements, etc.) Interventions to support adequate oxygenation: decreased energy expenditure - alternate periods of rest and activity. Maintain comfortable room temperature. Administer oxygen as needed Iron pills: should be taken with vitamin C to enhance absorption. Do not take with calcium because it inhibits absorption Causes of SIADH - ANSHead trauma Cerebral tumors (hypothalamus/pituitary) Meningitis Cerebral hemorrhage Pulmonary disease: COPD, TB, bacterial pneumonia Positive pressure ventilation Small cell lung cancer Spinal surgery BMT or stem cell transplants Medications: thiazide diuretics, tricyclic antidepressants, SSRIs, nicotine CBC normal values - ANSWBCs (5,000-10,000) Differential: Neutrophils: 50-70% Lymphs: 20-40% Monos: 2-8% Eos: 1-4% Pancytopenia: decrease in all cellular components of the bone barrow; caused by bone marrow suppression Continuous renal replacement therapy (CRRT) - ANSGradual over 8-24 hours Two types: Arterial venous: patient's own arterial hemodynamics remove the blood Veno-venous: utilizes external pumping device to move the blood Indications: AKI and hemodynamic instability Different types of CRRT based on patient's needs and condition. Ultrafiltration CRRT is mostly for water removal and does not use dialysate or replacement fluid. CRF clinical manifestations - ANSUremia - accumulation of wastes/toxins resulting in systemic symptoms Hematopoietic: anemia-decreased EPO production CV: CHF, HTN, dysrhythmias, pericarditis, edema Respiratory: pulmonary edema, infection Endocrine: altered glucose control, hypothyroidism GI: N/V, altered taste, increased GI acid production Neuro: decreased LOC, numbness, tingling, hyperreflexia, calcifications Skeletal: pruritus, delayed wound healing GU/reproductive: decreased ovulation and spermatogenesis Other: metabolic acidosis CRF labs - ANSIncreased Cr Increased BUN - BUN varies with fluid and diet so it is less reliable than Cr Uremia CRF stage 1 - ANSDiminished renal reserve: nephron destruction and compensatory hyperfiltration occurs. Typically asymptomatic, may have elevated BUN. GFR = 50% of normal function CRF stage 2 - ANSRenal insufficiency Attempts at compensation occurs but is inadequate to clear waste. BUN and Cr are elevated. Anemia and HTN are common GFR = 20-50% of normal function CRF stage 3 - ANSRenal failure Many organ systems are affected. Metabolic acidosis, azotemia, worsening anemia, severe alterations in electrolytes, fluid, and acid-base balance occur, requiring dialysis. Fluid excess is apparent. GFR is below 20% CRF stage 4 - ANSEnd-stage renal disease GFR: less than 5% CRF treatments - ANSDialysis Treat symptoms HTN: K-sparing diuretics, ACE inhibitors Anemia: EPO, iron supplements Correct electrolyte imbalances Fluid and dietary restrictions: low sodium, low protein, low potassium, low phosphate Oxygen to help hypoxia related to anemia Infection concerns CRRT nursing management - ANSStandard indicators to indicate how patient is tolerating treatment: weights, VS including hemodynamic stability Additional monitoring includes: monitoring lab values to ensure adequate fluid and electrolyte balance and checking/maintaining patency of the CRRT system D5W exception - ANSIsotonic then hypotonic (once inside the body) A carbohydrate solution that uses glucose as the solute dissolved in sterile water Packed as an isotonic solution, but becomes hypotonic once in the body because the glucose is metabolized rapidly by the body's cells Dehydration - ANSLoss of H2O from extracellular fluid volume Causes: Lack of fluid intake: cognitive impairment, decreased access to fluids, decreased thirst. Excess fluid loss: potent diuretics, severe V/D, fever, diaphoresis, hyperglycemia, hyperventilation, increased ADH, DI, Addison's, diuretic phase of ARF, GI suctioning, burns, etc. Symptoms: weight loss, thirst, decreased and concentrated urine output, weak pulse, decreased BP, postural hypotension, decreased CVP, dry mucous membranes, LOC changes, headache, decreased capillary refill, tenting skin Labs: high serum osmolality, high sodium, high BUN, high glucose, high HCT, high urine specific gravity Treatment: oral rehydration, IV hydration (isotonic usually), correcting nausea, monitoring lab values, monitoring U/O, and antipyretic agents Determining burn severity - ANSMust determine % BSA involved Depth of injury Age Associated or pre-existing disease Burns to hands, face, and genitalia are considered more severe. Also considered more severe when they are on a joint because the skin might not grow back correctly. Initial estimate: 1st, 2nd, 3rd degree determine thickness, while rule of 9's determine BSA (extent) DI interventions - ANSMonitor: daily weight (weight loss), I/O, vital signs (hypotension, tachycardia), neuro check, assess for sever thirst and dry mucous membranes Pharm: hypotonic solution and ADH replacement with DDVAP or vasopressin (ADH) Non-pharm: increase free water intake, surgery to remove tumor Teaching: teach patient and family about signs, symptoms including complications of DI DI labs - ANSSerum Osmo >300 Serum Na >145 Urine osmo <300 Urine specific gravity <1.005 DI medications - ANSDesmopressin: increased water reabsorption at the nephron. ADH analog. Potential adverse effects: nasal congestion, decreased Na, and decreased urine output Vasopressin (Pitressin): promotes reabsorption of water at the renal tubule. ADH. Potential adverse effects: decreased U/O, increased GI motility, increased BP (caution with h/o angina and MI) DI treatment - ANSFrequent neuro assessments Monitor intake/output hourly Monitor electrolytes (Na and Cl) Replace fluids hourly with hypotonic fluids (1/2 NS) mL/mL hourly replacement Hormonal replacement (DDVAP, vasopressin) Diabetes insipidus - ANSPassing of urine "without taste" - tasteless because of relatively low sodium content Occurs when secretion or action of ADH is abnormally low - hypothalamus produces insufficient ADH, posterior pituitary fails to release ADH, or nephron does not respond to ADH Results in severe dehydration, thirst, and hypernatremia Diabetes insipidus causes - ANS1. Central (decreased ADH) - damage to pituitary or hypothalamus from CNS tumors, TBI, CNS infections, or genetic disorder 2. Nephrogenic (kidney resistance to ADH) - acute tubular necrosis and lupus. Can be inherited or from medications (lithium, steroids, Dilantin, antibiotics). Can also occur from electrolyte problems such as hypercalcemia and hypokalemia 3. Gestational: enzyme made by the placenta called vasopressinase destroys vasopressin. Also destroys ADH in the mother. 4. Primary polydipsia: caused by abnormal intake of excessive fluids. Abnormal thirst caused by damage to the thirst-regulating mechanism in the hypothalamus Serum bicarbonate <18 mEq/L Moderate ketonemia or ketonuria Manifestation: polydipsia, polyuria, polyphagia, dehydration, dry mouth, tachycardia, changes in LOC, air hunger, acetone breath, increased RR, nausea, vomiting, Kussmaul breathing Endocrine function and aging - ANSEndocrine system functions well in most older people Some changes occur because of normal damage to cells during the aging process Hormone production and secretion Hormone metabolism (how quickly excess hormones are broken down and leave the body, for example, through urination), hormone levels circulating in blood, biological activities, target cell or target tissue response to hormones, rhythms in body, such as menstrual cycle Endocrine system - ANSCellular communication: tissues secrete hormones carried by blood to act on a target tissue Glands distributed throughout the body Erythropoiesis - ANSRBCs manufactured in the bone marrow. If you take a peripheral blood draw and find a large number of blast or baby cells, there is some sort of uncontrolled release of baby cells into circulation. Erythropoiesis is dependent upon the release of EPO from the kidney in response to blood cell oxygen demand. Also dependent on intake of nutrients and minerals. Reticulocyte count is an indicator of RBC production rate and EPO response Hemoglobin: made of iron (heme) and protein (globin). You can bind four oxygens to one hemoglobin molecule. RBCs live 120 days. IF someone has anemia that is unspecified, you will check reticulocytes, MCV, MCH, and MCHC to determine the type of anemia. Reticulocytes are new baby RBCs. The amount of reticulocytes can tell you how many RBCs are being produced in response to erythropoietin. Factors affecting the aging immune system - ANSStress: suppresses immune response because of chronic inflammatory state - also affects how your body responds to EPO and shortens the lifespan of RBCs Comorbidities: kidney failure, cardiac problems, nutrition issues, and liver issues Exercise: increases perfusion to organs, promotes production of RBCs, helps immune system function Nutrition: deficiencies in folic acid, protein, vitamins, etc. First degree - ANSSuperficial partial thickness. Sunburn Only involves the epidermis. Pain and redness, sensitive to air, no blisters. Heals in a few days - outer injured epithelial cells peel. Seldom clinically significant. Fluid compartments - ANSIntracellular compartment: rich in potassium, phosphate, and protein. Moderate amounts of magnesium and sulfate ions and Na because of Na/K pump Extracellular compartment: plasma proteins and water, Na and potassium Fluid resuscitation - ANS2-4 mL RL x kg x %BSA of burn 1/2 of the total fluid in the 1st 8 hours (starts at time of event) 1/4 of the total fluid in the 2nd 8 hours 1/4 of total fluid in the 3rd 8 hours Fluid resuscitation - ANSIV fluids are classified according to their osmolality or tonicity: refers to the number of milliosmoles per liter of solution. Refers to the effect that the solution has on the extracellular fluid and intracellular fluid compartments Gigantism - ANSToo much GH Onset in childhood Epiphyseal growth plates are active, so long bones will grow uncontrollably Glomerulonephritis - ANSGlomeruli: semi-permeable membrane which allows blood filtration. This is where urine formation begins. The amount of blood filtered each minute is the GFR, which is normally about 125 mL/min Inflammation of glomeruli: affects both kidneys equally and is the 3rd leading cause of ESRD in the US This inflammation of the glomeruli causes blood and protein to be lost in the urine. If left untreated, the chronic inflammation can lead to scarring, loss of kidney function, high BP, and kidney failure Can be acute or chronic. Acute: symptoms begin suddenly and can be temporary or reversible. Chronic: slowly progressive, typically leading to irreversible renal failure Glomerulonephritis labs - ANSUrine: proteinuria, hematuria, RBCs Serum: increased BUN, Cr Goiter - ANSNot diagnostic. Can be related to hyperthyroidism, hypothyroidism, and normal thyroid function Iodine intake: inadequate dietary iodine intake leads to an inability to synthesize TH. TSH stimulation continues, resulting in an enlarged thyroid gland Assessment: TSH and T4 levels are measures to determine if goiter is associated with hyperthyroidism, hypothyroidism, or normal thyroid function Management: high iodine diet - use iodized salt. Iodine will reduce the size and vascularity of the goiter. Can replace thyroid hormones until the deficiency goes away. Surgical management may be discusses with hyperthyroidism due to breathing and swallowing issues Hematopoiesis - ANSFormation and development of blood cells Prenatally, hematopoiesis occurs in the yolk sac, then the liver, and lastly in the bone marrow Hematopoiesis in adults occurs in the bone marrow and lymphatic tissues All types of blood cells are derived from stem cells that have the potential to develop into all types of blood cells. RBC, WBC, platelets. Hemodialysis - ANSAccess: dialysis catheter (short term); AV fistula (long term) Indications: BUN >90 & Cr >0 K > 6.0 Drug toxicity - gets drug out of the body quickly GFR <15 mL/min Metabolic acidosis Contraindications: hemodynamic instability, inability to coagulate, no access Requires a machine and access to blood. Hemolytic anemias - ANSDrug-induced: sulfonamides can cause destruction of RBCs Infectious Physical agent: burns Microangiopathy: damage occurs as RBCs move through the small damaged vessels Transfusions: when wrong blood type is infused Heparin-induced thrombocytopenia - ANSType I: transient decrease in platelets in patients on heparin therapy *Type II*: immune-mediated complication of heparin therapy which involves decreased platelets and thrombi formation (0.5-5% of patients treated with heparin) Risk factors: use of heparin, cardiac transplant patient, hemodialysis patient, and patents with orthopedic, cardiac, and neuro-related surgeries Onset of HIT: 5-14 days after initiation of heparin therapy - platelet count about 50,000- 80,000 Health complications resulting from HIT: CVA, MI, PE, arterial occlusion, DIC Ascites is also caused by a combination of elevated hydrostatic pressure in veins running through the liver (portal hypertension) and a decrease in colloid osmotic pressure due to decreased serum albumin due to liver failure Type I HRS is caused by decreased BP due to aggressive diuresis, large volume paracentesis, GI bleed, major surgical procedure or acute viral hepatitis Type II HRS is caused by severe ascites refractory to diuresis HRS interventions - ANSMonitor/assess: patient's mental status, daily weight, I/O, labs, and VS Pharm: administer albumin (for plasma expansion), lactulose (to correct ammonia), vasopressin (vasoconstriction to improve kidney function), low dose-dopamine to improve renal blood flow Non-pharm: low salt diet, safety precaution due to change in mental status. Do not restrict protein intake unless the patient has severe encephalopathy Teaching: importance of low sodium diet, need to report any signs of change in mental status HRS labs - ANSIncreased AST, ALT Decreased albumin Prolonged PT ARF labs HRS management - ANSFocused on supportive care for liver disease Fluid resuscitation CRRT Pharm: midodrine (peripheral vasoconstriction), octreotide (splanchic vasoconstriction), albumin (oncotic agent) Surgical: liver transplant, TIPS (transjugular intrahepatic portosystemic shunt) HRS patho - ANSPortal hypertension leads to splanchic vasodilation, leading to decreased effective circulatory volume, which activates the RAAS leading to renal sodium avidity (ascites) and renal vasoconstriction (HRS) The dilation of splanchic circulation (intestines) is caused by the release of mediators such as nitric oxide and prostaglandins from the cirrhotic liver Because of the dilation perfusion to the kidneys, the RAAS is activated. The blood vessels in the kidney circulation constrict to improve perfusion. However, the effect is insufficient to counteract the mediators of vasodilation in the splanchic circulation, leading to persistent "underfilling" of the kidney circulation and worsening kidney vasoconstriction, leading to kidney failure HRS symptoms - ANSType I: rapid, progressive (serum Cr doubles over 2 weeks) Type II: chronic, slowly progressive (slow increase of serum Cr) General: liver failure with increased LFTs - oliguria, decreased serum and urine Na, increased BUN and Cr, decreased GFR Hepatic encephalopathy occurs with liver failure due to the liver's inability to filter ammonia from the intestines out of the blood. Ammonia can cross the blood brain barrier and produce neurologic manifestations Abdominal swelling Change in mental status Confusion Delirium Dementia Coarse muscle movements, jerking Dark-colored urine Decreased urine production Nausea and vomiting Weight gain Yellow skin Hyperaldosteronism - ANSAldosterone conserves sodium and promotes potassium excretion Primary: hypersecretion of aldosterone secondary to adrenal lesion (usually benign) produces secondary HTN, hypernatremia, and hypokalemia Secondary: results from renal disease, laxative or diuretic abuse, dehydration, cirrhosis with ascites, and heart failure Clinical manifestations: Primary: may be asymptomatic, HTN, hypernatremia, hypokalemia - excessive urinary excretion - muscle weakness, cardiac dysrhythmias Hyperaldosteronism diagnosis and management - ANSDiagnosis: serum potassium levels, alkalosis, elevated urine or plasma aldosterone levels Management: Primary: spironolactone drug of choice - to increase sodium excretion, treat HTN, and improve hypokalemia Surgery: unilateral or bilateral adrenalectomy. Temporary/permanent replacement therapy Secondary: manage causative disease. Comply with treatment of disease Education: comply with treatment and maintain control of the causative disease process (secondary) Hypercortisolism - ANSHyperfunction of adrenal cortex, resulting in excessive production of glucocorticoids Cushing's syndrome: caused by medical interventions for most cases, adrenal tumor, or excessive ACTH secretion - pituitary hypersecretion secondary to pituitary tumor. Clinical manifestations: normal function of the glucocorticoids become exaggerated - poor wound healing, masculine characteristics in women, memory loss, poor concentration, persistent hyperglycemia (steroid diabetes), potassium depletion, sodium and water retention, HTN, abnormal fat distribution - moon-shaped face, fat pad on back of neck, obesity with slender limbs, purple striae on breasts and abdomen Hypercortisolism diagnostics and management - ANSDiagnostics: physical exam, clinical manifestations, ACTH levels, 24 hour urine collection for free cortisol. High dose dexamethasone suppression test - checks to see how taking corticosteroid medicine changes the levels of cortisol in the blood. CT and MRI on pituitary and adrenal glands Management: reducing corticosteroid use over time while still managing condition (asthma/arthritis) Medications that interfere with ACTH production or adrenal hormone synthesis such as Mitotane. Surgical: adrenalectomy - adrenal tumor. Even removal of one requires careful monitoring - remaining adrenal may have atrophied or stopped working Lifelong glucocorticoid mineralocorticoid replacement Most physical manifestations resolve after bilateral adrenalectomy Education: patients on glucocorticoids are at risk for Cushing's. Recognizing manifestations. Hyperglycemic hyperosmolar state - ANSHyperglycemic complication of diabetes that results from insulin deficiency and resistance. Characterized by extreme hyperglycemia, severe osmotic diuresis, and altered mental status. Generally a slow onset. HHS is seen in type 2, >65 years, HHS 5-10% Fatalities much more likely caused by comorbid conditions, rather than be directly caused by HHS Onset is slow and insidious. Those with type II diabetes who are older and obese with underlying CV conditions are at greatest risk Etiology: infection (pneumonia, UTI), stroke/MI, stress of illness, medications (corticosteroids) Hyperthyroidism treatment - ANSRemoval of thyroid tumors (surgery), administration of adrenergic blocking agents (control SNS activity) Administration of antithyroid medications: propylthiouracil - most commonly used and impairs TH synthesis. Radio iodine therapy (potassium iodide) to reduce vascularity and activity of thyroid before subtotal/total thyroidectomy. Given 10-14 days before surgery. Can also be used to treat thyroid storm. Radioiodine therapy destroys thyroid cells, so they will have to be on thyroid replacement therapy for the rest of their lives. Will need a high calorie diet due to hypermetabolic state. Salt reduction in order to reduce edema. Elevate HOB to decrease pressure on the eyes and instill eye drops. Education: for exophthalmos, wear dark eye glasses to reduce discomfort and reduce risk of getting dirt/dust in eyes Use sleeping mask or lightly tape eyes shut with paper tape. Elevate HOB at night to reduce edema Diet: restrict salt intake, high calorie/high protein, supplemental vitamins, and weigh daily Hypertonic solutions - ANSContain higher concentration of particles than exists in the intracellular and extracellular fluid Shifting fluids from the intracellular and extracellular into the intravascular compartment, expanding blood volume D10W, D5 1/2 NS, 3% NS Hyponatremia - ANSCauses: diuretics, vomiting, diarrhea, diaphoresis, renal failure, hypervolemia, SIADH Symptoms: N/V/D, hyperactive BS, decreased DBP, tachycardia, neuro symptoms, dry skin, pallor, dry mucous membranes Treatment: increase sodium to water ratio in ECF, hypertonic saline replacement (3% NaCl). Restrict fluids, normalize serum osmolality, assess volume status of patient, assess urine sodium concentration (for diagnosis purposes), and correct sodium at no more than 0.5 mEq/L per hour or 12 mEq/L per 24 hours Hypoparathyroidism - ANSHyposecretion of parathyroid glands Due to accidental removal of parathyroid glands or damage to these glands during thyroidectomy. Hypomagnesemia can cause a decrease in PTH secretion and function Serum calcium levels are low Serum phosphate is high Tetany (painful muscular spasms/tremors) may develop Patho: reduced PTH leading to slowed bone resorption, low serum calcium levels and increased serum phosphate levels. Absence of PTH causes impaired reabsorption of calcium from bone and of calcium from the renal tubules. Decreased serum calcium causes severe neuromuscular irritability. Diagnostics: physical exam, labs (low calcium, low PTH, high phos) Clinical manifestations (mainly from low serum calcium): painful muscle spasms, numbness, tingling, tingling on fingers/toes, dysrhythmias, Chvostek's sign and Trousseau's sign, patchy hair loss, dry skin, headaches, depression, memory loss Hypoparathyroidsm managament - ANSEmergency management: restore serum calcium levels to normal quickly with 10% calcium gluconate. Prevent and treat seizures Control laryngeal spasms and respiratory obstruction which may lead to distress - have trach tray easily accessible Long-term management: oral calcium salts, vitamin D, PTH replacement, diet high in calcium, but low in phos (beans, tofu, soy, nuts, oranges, broccoli, cabbage, sardines, and green leafy veg) Education: life-long medications. Visit healthcare provider to have calcium levels monitored. Dietary modifications: omit cheese and milk (high phos) Hypopituitarism - ANSVery rare. Can affect one or more of the pituitary hormones. Anterior pituitary: releases adrenocorticotropic hormone, thyroid stimulating hormone, follicle-stimulating hormone, leutenizing hormone, growth hormone, prolactin, and melanocyte stimulating hormone Posterior pituitary: secretes ADH and oxytocin. Most deficiencies associated with hypopituitarism involve GH and gonadotropins (LH,. FSH) due to a pituitary tumor Hypothyroidism - ANSUnder-activity of thyroid gland resulting from: Primary thyroid dysfunction: TH levels are low - TSH levels are elevated (thyroid is not responding). Most common form of primary hypothyroidism is Hashimoto's Disease - relatively rare, but is an autoimmune disease that results in thyroid gland atrophy Secondary thyroid dysfunction secondary to pituitary or hypothalamus dysfunction: decreased TSH levels AND decreased TH levels Decreased level of TH leads to: overall slowing of metabolic rate: Decreased secretion of HCl in stomach Decreased GI motility Bradycardia Slowed neurologic functioning Decreased heat production resulting in decreased body temperature Inadequate stimulation of RBC development in the bone marrow: anemia with possible vitamin B12 and folate deficiency Reduction in lipid metabolism, results in increased serum cholesterol and triglycerides (arteriosclerosis, CAD) Hypothyroidism management - ANSCorrect TH deficiency Reverse manifestations: most improve in 2-3 weeks with TH therapy Prevent further cardiac and arterial damage Patient/family education imperative: diet, iodized salt, high fiber, recognizing signs and symptoms of medical emergency, monitor weight, lifelong drug therapy needed/stressed. Must monitor drug levels to ensure adequate dosage. Hypothyroidism symptoms - ANSMild: Hair loss, anorexia, lethargy, dry skin, muscle aches and weakness, intolerance to cold, facial and eyelid edema, brittle hair and nails, forgetfulness, depression, small goiter that often leads to a doctor visit Severe: myxedema - develops in undiagnosed or undertreated clients that experience stress. Accumulation of hydrophilic mucopolysaccharides in dermis and other tissues - leads to puffiness, periorbital edema, and a masklike effect. Complicated: myxedema coma - triggered by stress or noncomplicance with thyroid treatment. Mortality rate is nearly 100%. Decrease in metabolic rate is so low that they get hypoventilation, hypothermia, hypotension, hyponatremia, hypercalcemia, hypoglycemia, and water intoxication. Management: vital functions are supported - airway, IV fluids, warmth, and vasopressors. IV levothyroxine, IV glucose, and IV corticosteroids (potential risk for precipitating acute adrenal insufficiency caused by the accelerated metabolism of cortisol following T4 therapy). Diagnostic: labs, TSH, T4, radioactive iodine uptake Hypotonic solutions - ANSContains a lower concentration of particles than exists in the intracellular fluid and extracellular fluid Shifts fluids from the intravascular compartment into the intracellular compartments 0.45% NS, 02% NS, 2.5% dextrose Immunoglobulins - ANSAKA antibodies are glycoprotein molecules produced by WBCs They act as a critical part of the immune response by specifically recognizing and binding to particular antigens, such as bacteria or viruses in aiding their destruction Increased blood loss anemia - ANSHemorrhage: post-op, trauma, anticoagulation Chronic bleeding: cirrhosis, colitis, diverticulitis, colon cancer, etc. Menstrual blood loss Major manifestations of anemia - ANSMild anemia: 10-12 g/dL Moderate anemia: 7-10 g/dL Fatigue, dyspnea, tachycardia/palpitations, diaphoresis with exertion Severe anemia: < 7 g/dL Dyspnea, palpitations at rest, dizziness/headaches, irritability, insomnia, hypersensitivity to cold, difficulty concentrating. Pallor, anorexia/indigestion, decreased urine output due to redistribution of blood. Long bone pain due to increased production of EPO. Neuro: vertigo, irritability, inability to concentration GI: anorexia Integ: pale skin and mucous membranes General: activity and temperature intolerance Management principles - ANSVital signs Insert NG tube Insert urinary catheter Assess extremity perfusion Ventilation status Pain relief: IM opioid administration is avoided because of the need for repeated, painful injections, and because of variable vascular absorption due to unpredictable compartmental fluid shifts and muscle perfusion in burn patients, particularly those undergoing acute, burn shock resuscitation Psychological assessment Manifestations of ARF - ANSMost common initial manifestation is oliguria - urine output less than 400 mL/day Elevated BUN and Cr Uremia: fatigue, anorexia, nausea, vomiting, pruritus, neuro changes Decline in GFR: anuria: <100 mL/24 hours, oliguria, azotemia (accumulation of urea nitrogen and creatinine in the blood) S3, S4, crackles, DOE, weight gain, edema, fluid overload Medical history - ANSPre-existing or associated disease Medications, ETOH, drugs Allergies Tetanus status AMPLE Allergies Medications Past medical history, illness, pregnancy Last meal or drink Events/environment related injury Must perform a complete head-to-toe examination Movement of fluid - ANSFluid moves by osmosis - movement of water across a semi permeable membrane Osmolality: refers to concentration of solute in body water and reflects a patient's hydration status Starling forces: osmosis and diffusion of body fluids move freely between the interstitial and intravascular compartments Hydrostatic pressure: the pressure exerted by fluid in the interstitial or capillary space against the cell wall Oncotic pressure: the pressure exerted by plasma proteins as their flow through the capillary or exist within the interstitial space Second and third space edema: pitting and non-pitting edema, ascites (third space) National patient safety goals - ANSIdentify patients correctly: use at least two patient identifiers (meds, treatment, blood products) Improve staff communication: read back information received verbally, use standardized abbreviations, timeliness of lab and diagnosis tests, standardized "hand off" communication; important test results to correct person ontime Use medications safely: label all drug containers, clinical reasoning/decision-making. Extra caution with patients on blood thinners. Know and educate patients about meds (current and newly added) Prevent infection: comply with hand hygiene guidelines, use evidence-based guidelines such as VAP prevention, CVC bundle, surgical site infection, and CAUTIs Check patients medicines: reconcile medications while inpatient with usual meds and discharge meds Identify patient safety risks: comprehension fall prevention, encourage pt family to be involved in their care, suicide assessment Recognize and response to changes in patient condition Prevent mistakes in surgery: correct surgery on correct patient at correct body location; surgical "time out" before procedure Negative feedback mechanisms - ANSGlucose is ingested and absorbed into the intestine and the level of glucose in the blood rises. Elevation of blood glucose concentration stimulates endocrine cells in the pancreas to release insulin. Insulin has the major effect of facilitating entry of glucose into many cells of the body - as a result, blood glucose levels fall. When the level of blood glucose falls sufficiently, the stimulus for insulin release disappears and insulin is no longer secreted Neural stimuli - ANSResults from arrival of neurotransmitter at the neuroglandular junction Hypothalamus (link between nervous and endocrine systems) Contains ANS centers that control the adrenal medullae Hypothalamus has neural connections with the posterior pituitary, that cause the release of oxytocin and ADH Neutropenia in leukemia - ANSAbnormal decrease in neutrophils (<1,000) Absolute neutrophil count formula: (bands + segs) x WBC count / 100 Normal ANC: 2500-5000 ANC <500 severely increases risk for infection Normal albumin - ANS3.5-5 g/dL Normal BUN - ANS10-20 mg/dL Normal calcium - ANS9-10.5 mg/dL Normal chloride - ANS98-106 mmol/L Normal CO2 - ANS23-30 mmol/L Normal creatinine - ANS0.5-1.3 mg/dL Normal inflammatory response - ANSMultiple systems activated to protect host from insult and limit the extent of injury and promote rapid healing Insult can be microbial, but also mechanical, chemical, ischemic Mediators involve multiple pathways - from molecular to systemic Normal magnesium - ANS1.3-2.1 mEq/L Normal phosphorous - ANS3.0-4.5 mg/dL Normal potassium - ANS3.5-5.0 mmol/L Normal PT - ANS10-13 seconds x1.5-2.0 if on warfarin therapy Normal PTT - ANS60-70 seconds This must occur in the absence of factors known to stimulate ADH secretion such as severe pain, hypotension, and stress Pathophysiology of sepsis/SIRS - ANSStarts with an insult to the tissue and activation of the immune response which causes: Excessive vasodilation: to increase nutrient delivery and increase surface area for cellular access for immune cells. Causes decreased SVR and hypotension. Increased microvascular permeability: to increase nutrient transport to tissue cells and allow cellular access to tissue injury. Causes fluid and protein leaks into interstitial spaces, decreased circulating blood volume, peripheral edema, and ascites. Excessive cellular activation: for phagocytosis, wound healing, and further mediator release. Causes increased mediator production, leukocyte production, tissue edema, and vasoconstriction Increased coagulation: to prevent blood loss and wall off the injury. Causes microthrombi in organs and capillary beds to form. Can lead to DIC. All of these EXCESSIVE responses cause maldistribution of blood volume, regional tissue hypoxia, anaerobic metabolism, and lactic acidemia. All of these could eventually lead to MODS. Peptides/amino acids - ANSMade from amino acid Transported in blood Binds to cell membrane receptors of target tissues Activate second messenger systems or ion channels More temporary effects - need a constant supply of these peptides Examples: antidiuretic hormone, calcitonin Peritoneal dialysis - ANSUse the patient's own peritoneal membrane to remove waste and water from the blood. Dialysate is infused through a catheter into the patient's own abdomen and "dwells" for a certain period of time (physician order), and then is drained out of the patient. Not as precise as hemodialysis. Can be better for some patients because they can have a little more freedom - do not need to go to a center. However, every time they access the catheter, they are at risk for infection. Membrane can become less compliant with long-term use. Pheochromocytoma - ANSA rare condition characterized by an adrenal medulla tumor that produces excessive catecholamines The tumor is benign in most cases The secretion of excessive catecholamines results in severe hypertension If undiagnosed and untreated, may lead to diabetes mellitus, cardiomyopathy, and death Manifestations: severe episodeic hypertension accompanies by classic triad of severe, pounding headache, tachycardia with palpitations and profuse sweating, and unexplained abdominal or chest pain Attacks may be provoked by many medications, including antihypertensives, opioids, radiologic contrast media, or tricyclic antidepressants. The treatment consists of surgical removal of the tumor Pituitary treatment - ANSTranssphenoidal hypophysectomy: surgical removal of pituitary gland - treatment of choice. ADH, cortisol, and thyroid hormone replacement must be taken for life Patient teaching is essential with hormone replacement therapy - need to be properly hydrated when taking ADH Nursing care: postoperatively includes avoidance of vigorous coughing, sneezing, and straining at stool. To prevent CSF leakage from where the sella turnica (sphenoid bone) was entered. Never place an NG or Dobhoff. Test excessive nasal drainage for CSF. Positive feedback mechanism - ANSWhen contractions start, oxytocin is released, which stimulates more contractions and more oxytocin to be released. Hence contractions increase in intensity and frequency. Production and release of oxytocin stops after baby is delivered Post renal causes - ANSObstructions that block the outflow of urine. When the flow of urine is obstructed, urine goes back into the renal pelvis, and impairs kidney function Causes include blood clots, tumors, calculi, urethral strictures, neurogenic bladder, BPH, and trauma Bilateral ureteral obstruction can lead to hydronephrosis (distention and dilation of the kidney) which increases hydrostatic pressure and tubular blockage which further causes a decline in kidney function Treat outlet obstruction. Monitor I/O, pain assessment, monitor lytes during diuresis, and give IV fluids Potential complications of DKA and HHS treatment - ANSGlucose should decrease by 50-70 mg/dL per hour Ketosis and acidosis elevate the serum potassium level by causing a shift of potassium from the intracellular to the extracellular fluid. As the acidosis resolves, the serum potassium level may fall dramatically Monitor closely in fluid resuscitation for complications of fluid overload Prerenal causes - ANSFactors that are external to the kidneys. A reduction in systemic circulation reduces blood flow to the kidneys. Prerenal conditions can lead to intrarenal disease if decreased perfusion is prolonged With this prolonged renal ischemia, the kidneys lose their compensatory ability and damage to the kidney tissue occurs Causes: excessive fluid loss (hemorrhage, severe burns, GI illness, polyuria), decreased renal perfusion (decreased cardiac output, third spacing, MI), vascular obstructions (embolus, tumor), drugs (ACE inhibitors, NSAIDs, angiotensin receptor blockers) Treat by restoring adequate circulation to the kidneys. Monitor I/O, symptoms of FVE, VS. Administer mannitol and colloid substances to draw fluid into vasculature Primary vs secondary endocrine disorders - ANSPrimary: affects the gland directly. The gland is not working properly Secondary: affects the pathway before the gland. Gland may be working fine, but not getting enough stimulation from another site Quality healthcare definition - ANSTreatment and care that is Safe: treatment helps patients and does not cause harm Effective: research shows that treatments have positive results Patient-centered: healthcare providers treat all patients with respect. This means taking into account each patient's values about heath and quality of life Timely: patients get the care they need at a time when it will do the most good Efficient: treatment does not waste doctor's or patien'ts money or time Equitable: everyone is entitled to high quality healthcare. This includes men and women of all cultures, income, level of education, and social status Renal failure diet - ANSProtein restriction - cannot excrete Na+ restriction K+ restriction Phos restriction Vitamin supplements (iron, folate, B12) Fluid restriction: 1000-1500 mL/day If on dialysis, high protein diet is beneficial Rhabdo labs - ANSCreatine phosphokinase high Myoglobulinuria Serum myoglobin positive Hyperkalemia Hyperphosphatemia Hyperuricemia Hypocalcemia -> cardiac arrhythmias Hyponatremia Increased lactic acid Rhabdo patho - ANSBreakdown of muscle fibers with leakage of myoglobin into systemic circulation. This leads to hypovolemia (water moves to the muscle, reducing fluid volume and leading to decreased blood flow to the kidneys) Scope of practice - ANSDefinition of the rules, regulations, and the boundaries within which a fully qualified practitioner with substantial and appropriate training, knowledge, and experience may practice in a field of medicine, surgery, or other specifically defined field Second degree - ANSPartial thickness Involves entire epidermis and portion of the dermis. Pain, blisters, moist, capillary refill still intact Uninjured dermis and epidermal appendages at risk Will use silver as an antiseptic. Must debride blisters or nonviable tissue to prevent infection. Sulfamylon cream is good for getting out the eschar because it penetrates the tissue. Is painful. Secondary survey - ANSAfter resuscitation efforts are well-established, complete head- to-toe assessment, H&P, and radiographic/lab studies. Must determine circumstances of the injury. Very important to know if the patient lost consciousness. Assess if abuse or neglect is possible. Sepsis - ANSEtiology: microbial infection in the blood, abscess, bacterial translocation in the gut, or instrumentation/catheterization Sepsis diagnosis - ANSBefore the initiation of antimicrobial therapy, at least two blood cultures should be obtained. At least one drawn percutaneously and at least one drawn through each vascular access device if inserted longer than 48 hours. Other cultures such as urine, CSF, wounds, respiratory secretions, or other body fluids should be obtained as the clinical situation dictates Other diagnostic studies such as imaging and sampling should be performed promptly to determine the source and causative organism of the infection. May be limited by patient stability. Procalcitonin: showed the best performance for differentiating patients with sepsis from those with SIRS not related to infection. PCT also differentiates between bacterial and viral sources of sepsis. C-reactive protein: measures the general levels of inflammation in the body SOFA scores: sepsis-related organ failure assessment score. Score based on six different scores, one each for respiratory, cardiovascular, hepatic, coagulation, renal, and neurological systems. SOFA scores are predictors of mortality. The higher the score, the larger the chance of mortality. Sepsis management bundle - ANSEvidence-based goals that must be completed within 24 hours for patients with severe sepsis, septic shock, and/or lactate >4 mmol/L Evaluation for adrenal insufficiency: Cortisol may become depleted because of stress, which will affect blood pressure, etc. Will test this using the STEM test - giving them a dose of corticosteroid and seeing if they react by producing more cortisol Recombinant human activated protein C for severe sepsis (still in research phase) Low tidal volume mechanical ventilation for ARDS - to avoid barotrauma due to low compliance from fluid leaking into the alveoli. Tight glucose control - high blood sugar can cause poor wound healing and poor perfusion. Plus bacteria like. glucose. Notes from CPD: Trickle feed to avoid translocation of bacteria from the gut. If you third space (anasarca), you will lose albumin. If you are only second spacing, (ISF and mild edema), you will not lose albumin. Will give vitamin K if you have a high PTT. Give cryoprecipitate for low fibrinogen. You can only give platelets to correct low platelets, not low clothing factors. Patient will have a high bili due to micro-emboli forming in the liver and spleen Sepsis manifestations - ANSGeneral: -Temp: >38.3 or <36 -Heart rate >90 -Tachypnea -Altered mental status -Significant edema or positive fluid balance >20 mL/kg over 24 hours Hemodynamic: -Systolic BP <90 mmHg or >40 decrease in SBP or MAP <70 -Cardiac index <3.5 L/min Tissue perfusion: -Decreased capillary refill or mottling -Lactate levels >2 mmol/L Inflammatory: -WBC >12,000 or <4,000, >10% bands -C-reactive protein levels >2 times normal Sepsis nursing priorities - ANSIneffective tissue perfusion Decreased cardiac output Deficient fluid volume Impaired gas exchange Anxiety Outcomes: Regain and maintain stable hemodynamic levels Maintain adequate circulating blood volume Regain and maintain blood gas parameters within normal limits by the end of the shift Verbalize increased ability to cope with stressors by the time of discharge Sepsis resuscitation bundle - ANSThe sepsis resuscitation bundle describes below, but must be accomplished within the first 6 hours of presentation for patients with severe sepsis or septic shock. Serum lactate must be measured Blood cultures obtained before antibiotics administered *Broad-spectrum antibiotics must be administered within 3 hours of ED admission and within 1 hour of non-ED admission. Fastest way to get antibiotics in is cefazolin IV push 10 mL diluted.* In the event of hypotension or lactate >4 mmol/L -Deliver an initial minimum of *30 mL/kg of crystalloid (or colloid)*. -Following initial resuscitation additional fluids guided by frequent reassessment of hemodynamic status -Apply vasopressors for ongoing hypotension In the event of persistent hypotension despite fluid resuscitation or lactate >4 mmol/L: -Achieve CVP of >8 mmHg (question of accuracy). When their CVP reaches 8, we will administer norepinephrine. If this still does not work, we will give vasopressors (work on the actual muscle of the vasculature, not just the CNS) -Achieve central venous oxygen saturation of >70% Severe sepsis - ANSSeptic shock is subset of severe sepsis. To be considered severe sepsis, must have more than 1 sign of organ failure. Heart will fail due to hypotension. Kidneys will fail due to hypo-perfusion (acute tubular necrosis). Other failures/symptoms that can occur are respiratory, hepatic, hematologic, CNS, and unexplained metabolic acidosis. Severe sepsis manifestations - ANSSepsis with organ hypoperfusion One of the following: SBP <90 mmHg despite fluid resuscitation Acute mental status change PaO2 <60 mmHg on room air and PaO2/FiO2 <300 Increased lactic acidosis Oliguria DIC or platelet <80,000 Liver enzymes >2 x normal Creatinine increase >0.5 mg/dL Absent bowel sounds Total bilirubin >4 mg/dL Coagulation abnormalities Thrombocytopenia Metabolic acidosis Complications: ARDS DIC interleukins. Generally manifested as a combination of vital sign abnormalities, including fever or hypothermia, tachycardia, and tachypnea. Sepsis is the same thing, but there is presence of microorganisms in a normally sterile site (blood) Bacteremia is cultivatable bacteria in the bloodstream Stabilization procedures - ANSPre-hospital or ED Stop the burning process Universal precautions Initiate fluid resuscitation Elevate burned extremities above the heart. Cover patient with clean, dry sheet to prevent hypothermia. Gently cleanse wound with sterile saline. NO ice or cold water soaks - can worsen the burn and harm the skin cells Chemical burns: brush powders from skin, flush with copious amounts of water, remove contaminated clothing. Eye irrigation, if involved. Exposure protection for ED personnel Steroids - ANSDerived from cholesterol Transported in blood by carrier proteins Diffuses across the cell membrane of target tissue and binds to cytoplasmic-binding protein Enters nucleus and alters DNA transcription Has more permanent effects Examples: estrogen, cortisol, progesterone, testosterone Strategies for reducing med administration errors - ANSClinical calculation competency: frequent reviews - confidence in calculating Adherence to protocol: 6 rights, checking pt identifiers, using visual prompts Use of visual reminders: posters, pictures, etc. Knowledge of medications: clinical judgment based on patient-centered and pharmacological knowledge Minimize distractions Time management 1. Proper patient identification 2. Adequate communication 3. Drug label reading 4. Use of drug delivery systems 5. Education: patient and staff 6. Double check high alert meds 7. Minimize interruptions during med administration 8. Minimize fatigue and sleep loss Symptoms of DI - ANSSymptoms onset 5-10 days after initial injury Polyuria: u/o 3-4 L/day (>200 mL/hr) Clear urine Bedwetting in children Polydipsia: intense thirst Excessive fluid intake Low urine osmolality Urine specific gravity <1.010 Hypernatremia (serum Na greater than 145 mEq/L) Serum becomes hyperosmolar - greater than 300mOsm/L Irritability or mental status changes Dry hands Constipation Irritability Dehydration Shock Decreased urine sodium Symptoms of SIADH - ANSLow urine output in absence of hypovolemia *Excessive thirst (same with DI)* Hyponatremia Low serum osmolality (<285 mOsm/L) High urine specific gravity Nausea and vomiting Weakness, fatigue, anorexia Altered LOC (increased ICP); seizures Muscle cramps/weakness Oliguria (<400 mL/24 hr) Increased weight WITHOUT edema Hypoactive reflexes Increased urine sodium Most of the symptoms are neuro: headaches, blurred vision, lethargy, apathy, disorientation, agitation, irritability Syndrome of inappropriate ADH - ANSIncreased production of ADH Increased water reabsorption in renal tubules, increased water retention and dilutional hyponatremia with a low serum osmolality The patient is hyponatremic, which would normally inhibit ADH secretion Third degree - ANSFull thickness Entire thickness of epidermis and dermis Decreased pain, blisters, dry, white, absent capillary refill Possible compartment syndrome if burn is circumferential due to inflammation being trapped under the leathery skin and inability to expand. Will require a skin graft Thrombocytopenia - ANSCauses: 1. Decreased production of platelets: medications (NSAIDs, chemotherapy), bone marrow injury, megaloblastic anemia 2. Increased destruction: immune-related (drugs, toxins, bacterial sepsis) 3. Increased utilization: idiopathic thrombocytopenia purpura (autoimmune platelet autoantibodies) 4. Distribution problems: splenomegaly associated with cirrhosis, leukemia, lymphoma, etc. Thyroid and thyroid hormones - ANSTake iodine, found in sea foods, meat, and iodized salt, and convert it to thyroid hormones, T4 and T3 Thyroid cells are the only cells in the body that can absorb iodine T3 and T4 are released into the bloodstream by stimulation of TSH and are transported throughout the body where they control metabolism (conversion of oxygen and calories to energy) T4 is converted to T3 in the cell. T3 can be used as an antidepressant Every cell in the body depends upon thyroid hormones for regulation of metabolism Thyroid hormone negative feedback: the amount of T4 produced by the thyroid gland is controlled by TSH. The amount of TSH that the pituitary sends into the bloodstream depends on the amount of T4 that the pituitary senses in the blood. If the pituitary senses little T4, it produces more TSH to tell the thyroid to produce more T4. Once the T4 gets to a certain level, the pituitary's production of TSH is shut off Thyroid storm - ANSThyrotoxicosis Can occur after a thyroidectomy or could happen with undiagnosed Grave's disease. Mostly happens in response to extreme stress: trauma, surgery, infection, stroke, etc. All hyperthyroid manifestations are heightened. HIgh fever, severe tachycardia, a-fib, delirium, dehydration, extreme irritability, tachypnea, distended neck veins, confusion, loss of consciousness, diarrhea, dehydration, and sweating. Potentially fatal acute episode characterized by increased metabolism and increased oxygen and energy consumption. Clinical diagnosis: know your patients - no lab tests differentiate hyperthyroidism from thyroid storm Management: hypothermia blankets (Tylenol will not work), IV fluids, suppressing hormone release (antithyroid drugs and corticosteroids), inhibiting hormone synthesis, blocking conversion of T4 to T3 with amiodarone, inhibiting effects of TH on body tissues (beta blockers), treat cause (if known) 5 B's: Block synthesis with antithyroid drugs Occluding the arterial blood flow in the arm with the blood pressure cuff for one to five minutes. If the thumb adducts and the phalangeal joints extend, it is positive Tumor lysis syndrome - ANSRapid tumor cell kill resulting from cancer therapy which causes rapid release of intracellular contents Tumor types at highest risk: Non-Hodgkins lymphoma, acute leukemias, CLL, and solid tumors such as small cell lung cancer and breast cancer. However, can occur in any tumor with a high proliferative rate, large tumor burden, or high sensitivity to cytotoxic therapy Two types of bone marrow - ANSYellow (adipose): produces fat, cartilage, and bone Red (hematopoietic): stem cell produces all three types of cell (RBC, WBC, platelets). Found in flat and irregular bones (end of long bones, pelvic, ribs, and more) Types of anemia with decreased RBC production - ANSIron deficiency anemia: can occur from poor intake or poor absorption (Chron's disease). Iron deficiency can cause pica (craving items that do not have nutritional value) Pernicious anemia: happens a lot with alcoholics - beefy red tongue, poor reflexes, confusion Aplastic anemia: bone marrow failure - pancytopenia Chemotherapy-induced anemia: temporary (usually within 2 weeks after chemo si stopped). Nadir is when they are at their lowest point of blood cells Anemia of inflammation: happens with chronic disease, chronic infections, or crucial illness causing decreased response to EPO and decreased survival rate of RBCs Types of immunoglobulins - ANSImmunoglobulin A: found in the mucous membranes lining the respiratory passages and GI tract, as well as in saliva and tears Immunoglobulin G: most abundant type of antibody - found in all body fluids and protects against bacterial and viral infections Immunoglobulin M: found in blood and lymph fluid. First antibody made when there is a new infection Immunoglobulin E: associated with allergic reactions Immunoglobulin D: least understood antibody - small amounts in blood Types of leukemia - ANSLeukemia is a malignant disease of the blood Can be acute or chronic and myeloid or lymphoid Myeloid: start in immature forms of myeloid cells - white blood cells (other than lymphocytes), red blood cells, or platelet-making cells. The most common form of adult leukemia. Can be kept in remission in approximately 60-70% of adults who undergo appropriate therapy Lymphoid: start in immature forms of lymphocytes (white blood cells). Lymphoid tissue is found in the lymph nodes, the thymus, spleen, tonsils, and adenoids, and is scattered throughout the digestive and respiratory systems and the bone marrow. The 2 main types of lymphocytes are T cells and B cells Acute: in acute leukemia, the bone marrow cells cannot mature properly. Immature leukemia cells continue to reproduce and build up. Without treatment, most people with acute leukemia would live only a few months Chronic: in chronic leukemia, the cells can mature partly but not completely. They also live longer, build up, and crowd out normal cells. Chronic leukemias tend to progress over a longer period of time, and most people can live for many years. Generally harder to cure than acute leukemias. Types of skin grafts - ANSAllograft: skin bank, foreskin, cadaver skin, temporary - will reject in 1-3 weeks Xenograft: skin harvested from other species like pig or baboon Synthetic skin: collagen matrix provides a scaffold onto which dermal cells can begin to grow Autograft: skin harvested from another site of the patient's body. Patient's own skin cells are grown in a lab. The best option Ultrafiltration - ANSan artificial method which mimics the ultrafiltration function of the kidneys. Blood is removed from the body and is passed through an extracorporeal circuit through a hemofilter and a predetermined percentage of plasma water is removed based upon a prescription. Typically, no more than 2 L an hour of fluid is removed. The remaining blood is returned to the patient. Unlike hemodialysis, hemofiltration, and hemodiafiltration, no dialysate or replacement fluids are used in SCUF. Vasoactive medication calculations - ANSFirst, find bag concentration If the dose is given in minutes, you have to times the dose by 60, then divide by the concentration. If the dose is given in hours, you do not have to do this. Formula is (dose x time) / concentration = rate Formula for finding dose is ([conc x rate] / weight) / 60 min = dose/kg/min