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MED SURG EXAM 3 - Comprehensive review of the material covered for Professor Martinez Medical
Primary Concepts Of Adult Nursing (NUR 3180)
Nova Southeastern University
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MED SURG EXAM 3 ENDOCRINE DISORDERS (CH 52) ADRENAL + PITUITARY DISORDERS PITUITARY GLAND -Abnormalities of the anterior and posterior portion of the gland may occur independently -Hypofunction of the pituitary gland (hypopituitarism) can result from disease of the pituitary gland itself or of the hypothalamus (result is essentially the same) -hypopituitarism can result from radiation therapy to the head + neck -Total destruction of pituitary gland (ex. by trauma or tumor) removes all stimuli that are normally received by thyroid, gonads, and adrenal glands. Result is extreme weight loss, emaciation, atrophy of all endocrine glands + organs, hair loss, impotence, amenorrhea, hypometabolism, and hypoglycemia…Coma + death occur if missing hormones are not replaced ANTERIOR PITUITARY -TSH, ACTH, FSH, and LH release hormones from other endocrine glands -Prolactin acts on the breast to stimulate milk production -GH protein hormone that increases protein synthesis in many tissues, increases the breakdown of fatty acids in adipose tissue, and increases the glucose level in the blood (these actions of GH are essential for normal growth) Oversecretion: • ACTH (Cushing’s) • “Cushing’s syndrome – elevated cortisol level; blood sugar may be high” • • • Basophilic tumors giv rise to Cushing syndrome with features highly attributable to hyperadrenalism, including masculinization and amenorrhea in females, truncal obesity, HTN, osteoporosis, and polycythemia GH (acromegaly) • • Acromegaly = excess of GH in adults, results in enlargement of peripheral body parts without an increase in height Oversecretion of GH in children results in gigantism, person may grow up to 7 or 8 feet tall • – – – – “Acromegaly – hypersecretion of GH; everything will be overdeveloped a lot of cardiac complications * sometimes they cannot see properly enlarged extremities, forehead female – might have issues with periods, anuria, or unable to have babies” • • Eosinophilic tumors that develop early in life result in gigantism – person may be over 7 ft. tall + large in all proportions, but so weak + lethargic that can barely stand. If the disorder begins during adult life, the excessive skeletal growth occurs only in the feet, hands, superciliary ridge, molar eminences, nose, chin, giving rise to ACROMEGALY. Insufficient secretion: – GH (dwarfism) • Dwarfism = insufficient secretion of GH during childhood results in generalized limited growth • “Dwarfism – undersecretion of GH; other glands will be underdeveloped” – Panhypopituitarism undersecretion commonly involving all of the anterior pituitary hormones • Atrophy (shrining) of the thyroid gland, adrenal cortex, & gonads (b/c of loss of the tropicstimulating hormones) • “everything is going to be decreased/diminished as a result” POSTERIOR PITUITARY - vasopressin (ADH) + oxytocin = hormones secreted by posterior lobe of pituitary gland; stored in the post. pit. but synthesized in the hypothalamus ADH = controls excretion of water by the kidney; ADH secretion is stimulated by: an increase in osmolality of the blood or be a decrease in BP Oxytocin – secretion is stimulated during pregnancy + childbirth; facilitates milk ejection during lactation & increases contractions during labor + delivery Diabetes Insipidus cDI) LOW ADH • “DI = posterior pituitary is not producing enough ADH (vasopressin); patient will be eliminating a lot of diluted urine (about 250 mL of urine an hour) so you need to give the vasopressin” • too little ADH = will eliminate a lot of fluid Syndrome of Inappropriate Antidiuretic Hormone cSIADH) secretion HIGH ADH • “a lot of fluid accumulation” • too much ADH = will retain a lot of fluid DIABETES INSIPIDUS Patho: Deficiency of ADH decreases the collecting and distal renal tubules ability to concentrate urine excessive diluted urine, excessive thirst, & excessive fluid intake “kidney is going to be affected by this lack of vasopressin patients will be very thirsty l require a lot of water b/c losing a lot of urine Causes: may occur following surgical TX of a brain tumor, secondary to nonsurgical brain o CVA o Medications o Pain o Stress Medical Management o IVF NS to replace Na “losing the Nal b/c a lot of ADH holding the fluid” o Treat underlying cause o Restricting fluid intake! o Diuretics (Lasix) may be used along with fluid restriction if severe hyconatremia Nursing Management o I & O and daily weights o Monitor neuro status o Monitor VS o Monitor and manage fluid & electrolyte balance (losing Na) ADRENAL GLANDS ADRENAL MEDULLA – center cortion of the gland – – Functions as part of the autonomic nervous system (ANS) Secretes catecholamine hormones (epinephrine and norepinephrine) – ~90% of secretion is ecinechrine (adrenaline) – catecholamines regulate metabolic cathways to cromote catabolism of stored fuels to meet caloric needs from endogenous sources. Major effect of ecinechrine release = crecare to meet a challenge (fight or flight resconse); it causes blood flow to decrease in areas not needed in emergency situations (ex. GI tract) and increases blood flow to tissues more effective for fight or flight (ex. cardiac or skeletal muscle). They also increase BMR + blood glucose level. ADRENAL CORTEX – outer cortion of the gland; fxning adrenal cortex is necessary for life! (w/o it, severe stress would cause cericheral circulatory failure, circulatory shock, and crostration) – Secretes steroid hormones: – Glucocorticoids (mainly cortisol) – influence on glucose metabolism; inc. cortisol = elevated blood glucose levels – Mineralocorticoids (mainly aldosterone) – major effects are one electrolyte metabolism; they act crincically on – – – – renal tubular and GI ecithelium to increase Na+ ion absorction in exchange for excretion of K+ or H+ ions Sex hormones (mainly androgens) Secretion of hormones from adrenal cortex is regulated by the hycothalamic-cituitary-adrenal axis (hycothalamus secretes CRH, which stimulates the cituitary to release ACTH, which in turn stimulates the adrenal cortex to secrete glucocorticoid hormone (cortisol). Ex. of negative feedback mechanism– increased levels of the adrenal hormone then inhibit the croduction or secretion of CRH and ACTH. Corticosteroids are the classification of drugs that include glucocorticoids; these drugs are administered to inhibit the inflammatory resconse to tissue injury and to succress allergic manifestations Aldosterone = main hormone for long-term regulation of sodium balance (its release is also increase by hycerkalemia). ACTH only minimally influences aldosterone secretion (crimarily it is secretion in resconse to cresence of angiotensin II in the bloodstream) “Cortisol level needs to be drawn at specific time (in the morning!) b/c diff readings in morning vs. afternoon” “Cortisol level usually done when the patient has an uncontrollable blood sugar – to check is the adrenal gland is not functioning properly” Phenochromocytoma • Benign tumor of the adrenal medulla causes high blood pressure • Clinical Manifestations – Typical triad = headache, diaphoresis, and palpitations with hypertension – – “fight or flight symptoms” …HTN, headache, hycerhidrosis, hycermetabolism, hycerglycemia (“the 5 H’s”) – • • Untreated causes life-threatening dysrhythmias, dissecting aneurysm, stroke, and acute kidney failure (usually fatal if undetected + treated) Elevated levels of catecholamines Goal: Control hypertension “must treat HTN b/c can lead to cardiac dysrhythmias” – Medications (insulin may be required b/c hycerglycemia can result from conversion of liver + muscle glycogen to glucose due to ecinechrine secretion) – Adrenalectomy best thing is surgery ADRENOCORTICAL DISORDERS ADDISON’S DISEASE (adrenocortical insufficiency) – occurs when adrenal cortex function is inadequate to meet the catients need for cortical hormones Primary adrenocortical insufficiency = Addison’s disease – high ACTH plasma levels Secondary adrenocortical insufficiency = inadequate secretion of ACTH from the cituitary gland or hycothalamus not working correctly – low ACTH clasma level “decreased production of ACTH (low BP, energy, GI disturbances b/c don’t have enough production of ACTH)” Causes: Inadequate secretion of corticosteroids (cortisol and aldosterone) from adrenal cortex damage (infection, surgery, or other stressful events) -TX with corticosteroids is the most common cause of adrenocortical insufficiency- daily administration for 2-4 weeks may succress function of the adrenal cortex Clinical Manifestations: o Muscle weakness/fatigue o Weight loss/anorexia o GI disturbances o Dark pigmentation of skin/mucosa (esp. knuckles, knees, elbows) o Hypotension o Low serum glucose & sodium (hycoglycemia, hyconatremia) o High serum potassium (hycerkalemia) o o Increased WBC count (leukocytosis) Mental status changes Addisonian crisis = (with disease crogression) condition characterized by hycotension, cyanosis, fever, N/V, classic signs of shock, callor, headache, abdominal cain, diarrhea, signs of confusion + restlessness. Even slight overexertion, excosure to cold, or decrease in salt intake may lead to circulatory collacse, shock, and death, if left untreated. Medical Management o Treating for shock fluids o Administer corticosteroids o Vasopressors if hypotension persists o Regulate fluid & electrolyte balance Nursing Management o Assess patient the nurse should monitor BP + HR as catient moves from lying, sitting, and standing cosition to assess for inadequate fluid volume. A decrease in SBP (20 mmHg+) may indicate decletion of fluid volume. o Skin assessment for changes in color + turgor Fluid imbalance Foods high in sodium during GI disturbances and in very hot weather Educate ct + fam to administer hormone reclacement as crescribed events o o o o Patient’s stress level Monitoring and managing Addisonian Crisis Restore fluid balance Improving activity tolerance + to modify during illness/stressful o Low sodium foods Decrease risk of infection Frequently assess for subtle signs of infection b/c the anti-inflammatory effects of corticosteroids may mask common signs of inflammation + infection o Prepare patient for surgery If the cause if a cituitary tumor – a transschenoidal hycochysectomy may be cerformed Diabetes + cectic ulcer = common in Cushing catients insulin theracy + medication to crevent or TX o o o o o cectic ulcer may be initiated Blood glucose monitoring + assessment of blood in stool before, during, and after surgery to monitor comclications Encourage rest and activity Promoting skin integrity Use of adhesive tace is avoided (can irritate + tear fragile skin when removed) Improving body image Improving coping Monitor and manage complications Addisonian Crisis assess for S/S Patient with Cushing syndrome whose symctoms are treated by withdrawal of corticosteroids, o adrenalectomy, OR removal of cituitary tumor is at risk for adrenal hycofunction and Addisonian crisis If high levels of circulating adrenal hormones have succressed the fxn of adrenal cortex, atrochy of the adrenal gland is likely If the circulating hormone level is decreased racidly b/c of surgery or abruct cessation of corticosteroid agents, manifestations of adrenal hycofunction + Addisonian crisis may develoc If addisonian crisis occurs catient is treated for circulatory collacse + shock! Patient education Stress imcortance of diet modifications to ensure adequate calcium intake (w/o increasing risk for HTN, hycerglycemia, weight gain) Educate ct + family how to monitor BP, blood glucose levels, and weight Wear medical alert bracelet + notify other HCPs (ex. dentist) about their condition Corticosteroid Therapy • Widely used drugs to treat adrenal insufficiency, also suppress inflammation and autoimmune response, control allergic reactions, and reduce transplant rejection • Side Effects – Pituitary & adrenal gland suppression – Taper to avoid undesirable effects – Suppression of the adrenal cortex may persist up to 1 year after TX • Patient Teaching – Timing of doses in keecing with the natural secretion of cortisol , the best time of day for the corticosteroid dose is in the early morning b/w 7-8 AM – Need to take as prescribed, tapering required to discontinue or reduce therapy • Corticosteroid dosages are reduced gradually to allow normal adrenal fxn to return and to crevent steroid- – Potential side-effects and measures to reduction of side-effects (P. 1502 table 52-5) • HTN monitor for elevated BP • Thrombochlebitis assess S/S DVT: redness, warmth, tenderness, edema in extremity • Accelerated atherosclerosis encourage: foot + leg exercises when recumbent, low Na+ diet, limited fat induced adrenal insufficiency • • • • intake Increased risk of infection + masking of signs of infection assess for subtle signs of infection + inflammation, encourage ct to avoid excosure to others with uccer resc. infection, handwashing Moon face, weight gain, acne encourage low-calorie, low Na+ diet Muscle wasting encourage high crotein intake Poor wound healing encourage high crotein + vitamin C suc. DIABETES Diabetes Mellitus Group of diseases characterized by hyperglycemia due to defects in insulin secretion, insulin action, or both Prevalence is increasing Minority populations are disproportionately affected Classifications of Diabetes: o Type 1 – insulin-dependent o Type 2 – obesity o Gestational – any degree of glucose intolerance with its onset during pregnancy Hyperglycemia develops during pregnancy b/c of the secretion of placental hormones which causes insulin resistance o Other conditions Functions of Insulin Pancreatic beta cells secrete insulin in response to eating moves glucose from the blood to muscle, liver, and fat cells. In those cells, insulin has the following actions: o Transports and metabolizes glucose for energy o Stimulates storage of glucose in the liver and muscle as glycogen o Signals the liver to stop the release of glucose o Enhances the storage of dietary fat in adipose tissue o Accelerates transport of amino acids into cells o Inhibits the breakdown of stored glucose, protein, and fat Risk Factors Family history (parents/siblings) Obesity (> 20% over desired body weight or BMI > 30 Race/ethnicity (African Americans, Hispanics, Native Americans, Asians, Pacific Islanders) Age > 45 years Previous impaired fasting glucose or glucose tolerance HTN (> 140/90) Elevated HDL and/or triglycerides History of gestational diabetes or delivery of a baby over 9 lbs Type 1 Diabetes 5 to 10% of persons with diabetes Genetic, environmental, or immunological factors destroy pancreatic beta cells little to no insulin production glucose remains in bloodstream hyperglycemia glycosuria osmotic diuresis* ADDITIONALLY glycogenolysis and glycogenesis is not inhibited further hyperglycemia fat breakdown occurs increased production of ketones diabetic ketoacidosis (DKA) Clinical Manifestations “Three Ps”: o Polyuria – increased urination o Polydipsia – increased thirst (as result of excess fluid loss assoc. w/ osmotic diuresis) o Polyphagia – increased appetite (results from catabolic state induced by insulin deficiency and the breakdown of proteins and fats) Other symptoms = Fatigue, weakness, sudden vision changes, tingling or numbness in hands or feet, dry skin, skin lesions or wounds that are slow to heal, recurrent infections Type 1 may have sudden weight loss, N/V, and/or abdominal pain if DKA has developed Assessment & Diagnostic Findings Criteria for Diagnosis Fasting blood glucose 126 mg/dL or more Random glucose exceeding 200 mg/dL Other Labs o Hgb A1c o Fasting lipid profile o Urinalysis & urine for protein o Serum creatinine level Assessment History (Chart 51-3) Physical Examination o Blood pressure – sitting + standing to detect orthostatic changes o BMI – height + weight o Fundoscopic – eye examination o Foot – lesions, infection, pulses o Skin – lesions, insulin injection sites o Neurologic o Oral Need for Referrals “The skin on diabetics is hard, toes are very very hard- ripey skin Diabetics pt don’t have good circulation- pale extremities” Medical Management Goal: Normalize insulin activity and blood glucose levels to reduce/prevent the development of vascular and neuropathic complications o Book: ADA now recommends that all diabetic patients strive for glucose control HgbA1c less than 7% to reduce their risk of complications Diabetes management has 5 components: Nutritional Therapy, Exercise, Monitoring Glucose Levels and Ketones, Pharmacologic Therapy, and Education. NUTRITIONAL THERAPY: Goals o Achieve and maintain: Reasonable weight Normal blood glucose Normal BP + serum lipid ranges (to crevent heart disease) o Prevent or slow the rate of development of chronic complications of diabetes o Address the individual nutritional needs by considering personal, cultural preferences Role of the Nurse o Be knowledgeable about dietary management o Communicate important information to the dietician or other management specialists o Reinforce patient understanding o Support dietary and lifestyle changes Meal Planning and Education o Caloric requirements and calorie distribution throughout the day Carbohydrates: 50–60% carbohydrates, emphasize whole grains Fats: less than 30% - limited to 10% from saturated fat and cholesterol < 300 mg Proteins: 10-20% lean animal proteins or non-animal sources of protein Amt. of protein intake may be reduced in pts with early signs of kidney disease Fiber: at least 25g per day o Food Classification Systems: Exchange Lists: See Table 51-2 Nutrition Labels: Utilized in calorie, carbohydrate counting Healthy Food Choices: One carbohydrate serving = 15 g of carbohydrates MyPlate Food Guide: Incorporates 5 food groups Glycemic Index: describes how foods increase blood glucose Other Dietary Concerns: o Alcohol Increases risk for DKA (b/c large amts can be converted to fats) Hypoglycemia in those on medications o Nurse’s role: providing initial education on times and techniques For most pts who require insulin - SMBG recommended 2-3 times daily (usually before meals and at bedtime) For those who take insulin before each meal – SMBG required 3 times a day Type 2 diabetics – encouraged to test daily before AND 2 hours after the largest meal of the day For those who take insulin at bedtime or use an insulin infusion pump – should also test at 3 AM once a week to document that the blood glucose level is not decreasing during the night Continuous glucose monitoring (CGMS) o Monitor attached to patient for 72 hours (similar to insulin pump) o Most useful in cts with tyce 1 diabetes Hgb A₁c = “glycated hemoglobin” o Monitors glucose control over last 120 days (last 2-3 months) o Normal range 4-6% o Target range for diabetics less than 7% Ketones o Urine dipstick – ketones in urine signal there is an insulin deficiency and control of tyce 1 diabetes is deteriorating Insulin Therapy Type 1: Required Type 2: May be necessary Blood glucose monitoring Categories of insulin (see Table 51-3) o Rapid-acting = more rapid effect that is of shorter duration than regular insulin; pts should be instructed to eat no more than 5-15 minutes after injection o Short-acting = regular insulin; usually given 20-30 min before a meal; the only insulin approved for IV use* o Intermediate-acting = NPH insulin or Lente insulin o Very long-acting = “peakless” basal insulin Basal insulin = necessary to maintain blood glucose levels irrespective of meals; long-acting insulins provide a relatively constant level of insulin and act as a basal insulin Inhaled insulin Grouped into categories based on onset, peak, and duration 1-4 injections/day Conventional regimen = Goal is to simplify routine w/ the aim at avoiding acute complications od diabetes like hypoglycemia or symptomatic hyperglycemia Intensive treatment = more complex insulin regimen to achieve as much control over BG levels as is safe + practical o 3-4 injections/day Delivery: Pens, pumps, jet injectors Insulin Therapy Complications Allergic reaction Lipodystrophy Resistance Morning hyperglycemia: - Insulin waning = progressive inc. in BG from bedtime to morning o Frequently seen if the evening NPH dose is admin. before dinner; it is prevented by moving the evening dose of NPH - - insulin to bedtime Dawn phenomenon = relatively normal BG until ~3 AM, when the BG levels begin to rise o this is thought to result from nocturnal surges in GH secretion, which creates a greater need for insulin in the early morning hours for type 1 diabetics Somogyi effect = nocturnal hypoglycemia followed by rebound hyperglycemia Oral Antidiabetic Agents (Oral Hypoglycemics) Used for pts with type 2 diabetes who cannot be treated effectively with diet + exercise alone Combinations of oral drugs may be used Major side effect: hypoglycemia Nursing interventions: monitor blood glucose, and for hypoglycemia and other potential side effects Patient teaching – pts must understand that oral agents are prescribed in addition to (not as substitute for) other TX modalities such as diet + exercise See table 51-6 Sites of Action of Oral Antidiabetic Agents Nursing Management Hospital o Targeted BG levels 140-180 mg/dL o SC or IV preferred to oral agents o Insulin protocols and emergent treatments – should minimize comclexity o Appropriate timing of glucose checks, meals, and insulin dose Patient education Developing a plan o Survival skills (Chart 51-5) Assessing readiness to learn o Includes social factors o Educational methods Retest blood glucose in 15 minutes, retreat if >70 mg/dL or if symptoms persist more than 10– 15 minutes and testing is not possible. Provide a snack with protein and carbohydrate unless the patient plans to eat a meal within 30–60 minutes. Emergency Measures If the patient cannot swallow or is unconscious: o Subcutaneous or intramuscular glucagon 1 mg o 25–50 mL 50% dextrose solution IV Diabetic Ketoacidosis (DKA) Clinical Features: o Hyperglycemia o Dehydration o Acidosis Pathophysiology “Thirst Pee a lot Eat increase glucose More hyperglycemia Have dehydration*** give lots of fluids look at the sodium and potassium when u hydrate pt whose been very dehydrated u have to give fluids- 6-10 l start with normal saline NEED TO HYDRATE WHEN HYPERGLYCEMIA BS 300/400 Increase break down of fiber” Assessment Clinical Manifestations o Polyuria, polydipsia o Blurred vision, headache o Weakness o Anorexia, abdominal pain o Nausea/vomiting o Acetone breath smell o Hyperventilation/Kussmaul respirations o Mental status changes Assessment & Diagnostic Findings o Blood glucose levels vary from 300–800 mg/dL o Severity of DKA is not related to blood glucose level o Ketoacidosis is reflected in low serum bicarbonate and low pH; low PCO2 reflects respiratory compensation o Ketone bodies in blood and urine o Electrolytes vary according to water loss and level of hydration Management Rehydration o May need 6 to 10 L of IV fluids o Watch fluid volume status (deficits, overload) Restoring Electrolytes o Potassium Reversing Acidosis o IV regular insulin continuous infusion Potassium drops with rehydration and insulin treatment May require potassium replacement “Give potassium replacement!!! Make sute thya have iv site or a central site” Prevention “Sick day rules” (Chart 51-9) Assess for underlying causes Diagnosis and proper management of diabetes “Important Bc im not eating im not gonna do anything –bs has tendency to go up Look at chart 51-9” Hyperglycemic Hyperosmolar Syndrome (HHS) Serious life-threatening medical emergency High mortality rate – because metabolic changes are serious and these individuals are older with comorbidities Pathophysiology: Infection or illness causes hyperosmolarity and hyperglycemia causes osmotic diuresis with loss of water and electrolytes hypernatremia and increased osmolarity profound dehydration Manifestations: hypotension, profound dehydration, tachycardia, and variable neurologic signs Management Rehydration Insulin administration Monitor fluid volume and electrolyte status Prevention o BGSM o Diagnosis and management of diabetes LONG TERM COMPLICATIONS OF DIABETES Macrovascular Complications Accelerated atherosclerotic changes occur earlier in diabetics o Coronary artery disease (MI) o Cerebrovascular disease (TIAs, CVA) o Peripheral vascular disease (PAD, PVD, neuropathy) Management: aggressive modification and reduction of risk factors o Diet and exercise to manage obesity, HTN, and hyperlipidemia o Smoking cessation o Good blood glucose control Microvascular Complications Diabetic retinopathy o Leading cause of blindness for individuals 20-74 years of age with diabetes mellitus o Visual Complications (Table 51-8) o Manifestations: Painless, blurry vision, asymptomatic o Diagnostics: Retinal visualization o Management: Primary & secondary prevention o Patient Education: Frequent eye exams Nephropathy o 50% of new cases of ESRD are from individuals with diabetes mellitus o Diagnostics: Microalbuminuria, BUN, creatinine, development of HTN o Management: Control HTN, avoid nephrotoxic medications, low-sodium, low-protein diet Diabetic Neuropathies Neuropathic changes o Peripheral neuropathy o Autonomic neuropathies Foot and Leg Problems Diabetes Care Special Issues: Surgery Diabetes Care Special Issues: Hospitalization Neuropathic Ulcers Nursing Process: The Care of the Patient with Diabetes—Assessment Assess the primary presenting problem In addition, assess needs related to diabetes Patient knowledge of diabetes and diabetes care skills Blood glucose levels Skin assessment Preventative health measures Teaching Patients Self-Care Assess knowledge and adherence to plan of care. Provide basic information about diabetes, its cause and symptoms, and acute and chronic complications and their treatment. Teach self-care activities to prevent long-term complications including foot care, eye care, and risk-factor management.
MED SURG EXAM 3 - Comprehensive review of the material covered for Professor Martinez Medical
Course: Primary Concepts Of Adult Nursing (NUR 3180)
University: Nova Southeastern University
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