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NUR 313: Adult Health - Study Guide

by: Courtney Erika

NUR 313: Adult Health - Study Guide NUR 313

Marketplace > Arizona State University > Health Sciences > NUR 313 > NUR 313 Adult Health Study Guide
Courtney Erika
GPA 3.7
Adult Health

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Adult Health
Study Guide
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This 18 page Study Guide was uploaded by Courtney Erika on Tuesday October 21, 2014. The Study Guide belongs to NUR 313 at Arizona State University taught by Flogel in Fall. Since its upload, it has received 328 views. For similar materials see Adult Health in Health Sciences at Arizona State University.


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Date Created: 10/21/14
Nur313 Exam 1 Study Guide Professionalism Illness and Stress Patient Teaching Nursing Process ppt1 82514 Far more people are in the hospital for exacerbations of existing chronic conditions than for acute injuries Behavior accounts for 40 of Determinants of Health ie smoking sedentary lifestyle poor nutrition EHOH cultural competence ability to understand and work effectively with patients colleagues and others whose beliefs values and history differ from your own Preventative health behaviors Primary exercise dietary intake non smoking good sleep patterns Secondary testing screenings bloodwork cholesterol mammograms Tertiary things to avoid a worsening condition rehab etc Increased life expectancy 778 for men 808 for women Agerelated changes Drugreceptor interaction drug receptors become more sensitive Metabolism metabolism drops 12 to 23 that of a young adult enzymes lose their ability to process some drugs making their half life longer Absorption gastric emptying slows as does absorption capacity of GI cells Circulation vascular nerve control is less stable Excretion renal blood flow GFRamp reabsorption decline Distribution total body water declines plasma protein levels decrease Medicare gt65 yo vs Medicaid poor 4050 of all hospitalizations are covered by Medicare Fightor Flight reaction sympathetic nervous system heart increased rate increase SV increase CO amp increased systolic BP blood vessels peripheral vasoconstriction redistribution of blood to vital organs lungs increased respiration amp shallow breathing adrenal medulla increased epinephrine amp norepinephrine prolonged SNS response liver glycogenolysis increased blood glucose GI system decreased secretions amp peristalsis decreased digestion ECG AssessmentDysrhythmias ppt 2 82514 dysrhythmia any abnormal rhythm must be immediately addressed NORMAL BLOOD FLOW gt SVC amp IVC gt right atrium gt tricuspid valve gt right ventricle gt pulmonary valve gt pulmonary artery gt lungs gt pulmonary veins gt left atrium gt bicuspid valve gt left ventricle gt aortic valve gt aorta gt systemic circulation electrocardiogram monitoring monitors electrical impulses in the heart ECG waves represent activity of charged ions across membranes of myocardial cells Calculating heart rate count R R segments over the 6 second interval amp times by 10 Normal sinus rhythm NSR HR 60100 PQRST all present Sinus bradycardia lt60 bpm with all other NSR Sinus tachycardia gt100 bpm with all other NSR Atrial Flutter atrial TACHYdysrhythmia originating from single ectopic focus regular sawtoothshaped flutter waves risk of stroke due to thrombus in the atria treat with Warfarin ALWAYS a P wave problem as seen by the repeated P wave Atrial Fibrillation total disorganization of atrial electric activity due to multiple ectopic foci result is loss of effective atrial contraction most common dysrhythmia increases with age severe decrease in cardiac output especially to systemic circulation QRS complex is the only recognizable complex on ECG atrial thrombi as a result of blood stasis embolus may develop and travel to the brain CVA treatment Warfarin amp cardioversion Fluid Electrol tes Acid Base Balance t3 8262014 Water content in the body adults 5060 older adults 4555 infants 7080 Intracellular fluid ICF lONS potassium and phosphate Extracellular fluid ECF ECF intravascular plasma interstitial ONS sodium and chloride Electrolytes measured in mEq Regulation of water balance hypothalamic pituitary adrenal cortical renal cardiac GI insensible water loss Goal homeostasis If you see one electrolyte out of normal limits expect to see others bring them back into normal range slowly and carefully Extracellular Fluid lmbalances Hypervolemia ECF volume excess excessive intake of fluids abnormal retention interstitialtoplasma fluid shift Nursing management remove fluid without changing electrolyte composition Hypovolemia ECF volume deficit abnormal loss of normal body fluids inadequate intake or plasma tointerstitial fluid shift Nursing Management replace water amp electrolytes quickly so as to avoid dehydration Assess skin turgor tenting dry mucous membranes peripheral pulses tachycardia BP low decreed urine output tachypnea daily weight neurologic function Sodium 135145mEqL Affects acidbase balance generationtransmission of nerve impulses ECF volume amp concentration Hypernatremia gt145 mEqL too much sodiumtoo little water or BOTH SS thirst lethargy agitation seizures from overstimulated neurons Treat non saline or hypotonic saline IV solutions to increase watersodium level or diuretics to pull sodium from the cells Hyponatremia lt135 mEqL water excess causing loss of sodium containing fluids SS confusion nausea vomiting seizures coma all difficult to decipher from hyper Treat IV hypertonic drugs that block Vasopressin saline fluid restriction Potassium 3550 mEqL major ICF cation Affects transmissionconduction of nerve amp muscle impulses cellular growth maintenance of cardiac rhythm acidbase balance regulated by the kidneys Hyperkalemia gt50 mEqL causes 1 kidney dysfunction adrenal gland disease movement of K out of cells into ECF meds SS cramping leg pain weak or paralyzed skeletal muscles V fib or cardiac standstill abdominal cramping or diarrhea Treat eliminate K from diet diuretics dialysis Kayexalate Hypokalemia lt35 mEqL causes abnormal losses of K via kidneys or GI tract magnesium deficiency metabolic alkalosis SS cardiac dysrhythmias skeletal muscle weakness respiratory weakness decreaed GI motility Interventions put on a heart monitor listen to heart sounds call the doctor keep Pt in bed to avoid falls 02 sat no deep breathing poor appetite constipation Treat KCI oral or IV must be diluted otherwise veinous collapse and pain so NO IV PUSH OR BOLUS no more than 1020 mEqhr to prevent cardiac arrest Calcium 86102 mEqL regulated by PTH and calcitonin Affects transmission of nerve impulses myocardial contractions blood clotting formation of teeth and bone muscle contractions Hypercalcemia gt102 mEqL causes hyperparathyroidism 67 of all cases malignancy vitamin D overdose prolonged immobilization SS decreased memory confusion disorientation fatigue constipation Treat plan ambulation activities excretion of Ca with loop diuretic hydrate with isotonic saline synthetic calcitonin Hypocalcemia lt86 mEqL causes decreased production of PTH acute pancreatitis multiple blood transfusions alkalosis decreased intake SS positive Trousseau s tetany of handwrist muscles positive Chvostek s cheek tetany of facial muscles laryngeal stridor dysphagia tingling around the mouth or in the extremities Treat oral or IV calcium supplements no IM to avoid local rxns treat pain amp anxiety to prevent hyperventiation induced respiratory alkalosis Magnesium 1525 mEqL coenzyme in metabolism of protein and carbs with 5060 contained in bone absorbed in GI amp secreted by the kidneys Affects myoneural junction neuromuscular excitability and contractility including cardiac function important for normal cardiac function Hypermagnesemia usually only seen during LampD to stop premature uterine contractions causes increased intake of magnesium during renal insufficiencyfailure amp excess IV mag administration SS lethargy nausea amp vomiting impaired reflexes somnolence respiratory and cardiac arrest Treat IV calcium chloride or calcium gluconate fluids to promote urinary excretion have 02 ready to administer to ensure the few breaths they are taking are oxygen rich Hypomagnesemia causes prolonged fasting or starvation chronic alcoholism fluid loss from GI tract prolonged parenteral nutrition without supplementation diuretics SS confusion hyperactive deep tendon reflexes tremors seizures cardiac dysrhythmias Treat oral supplements increase dietary intake parenteral IV or IM magnesium when SGVGFG IV Fluids Hypertonic more electrolytes than water initially expands and raises osmolality of ECF requires frequent monitoring BP lung sounds sodium level 10 Dextrose D10 D5 NS D5 12NS common maintenance fluid D5LR D1 OW free water Isotonic expands only ECF no net loss or gain from ICF 5 Dextrose in water D5W D5 Isotonic quickly metabolized to hypotonic Does not provide electrolytes Used to replace water loss Free water moves into ICF increases renal solute excretion 09 NaCl saline lsotonic more NaCl than ECF expands IV volume preferred for immediate response risk for fluid overload higher Does not change ICF volume Compatible with most meds blood products Lactated Ringers similar to plasma expands ECF Hypotonic give when dehydrated more water than electrolytes pure water lyses RBCs water moves from ECF to ICF usually MAINTENANCE 25 Dextrose 045 NaCl 12NS Acid Base Balance Buffers chemically neutralize acids Respiratory system eliminates CO2 increased respirations leads to increased elimination of CO2 and decreased blood CO2 responds in minutes to hours to changes in acidbase Renal system primarily reabsorbs CO3 eliminates H reabsorption and secretion of electrolytes responds within hours to days Alterations imbalances occur when compensatory mechanisms fail respiratory alterations affect carbonic acid H2CO3 metabolic alterations affect bicarbonate CHO3 Respiratory Acidosis carbonic acid excess caused by hypoventilation or respiratory failure compensation kidneys conserve bicarbonate HCO3 and secrete H into urine Respiratory Alkalosis carbonic acid caused by hyperventilation or hypoxemia from acute pulmonary disorders compensation rarely occurs because of aggressive treatment of hypoxemia Metabolic Acidosis base bicarbonate deficit cause by ketoacidosis makes your blood acidic lactic acid accumulation shock severe diarrhea kidney disease Metabolic Alkalosis base bicarbonate excess caused by prolonged vomiting or gastric suction gain of HCO3 compensatory mechanisms decrease respiratory rate to increase plasma CO2 renal excretion of bicarbonate HCO3 ABGs small amount of blood drawn from an artery common in ICU used for respiratory patients mostly evaluate pH analyze PaCO2 partial CO2 analyze HCO3 bicarbonate determine of CO2 or HCO3 matches the alteration decide if the body is attempting to compensate Anemia anemia is not a specific disease RBCs carry 02 from lungs to the tissue and CO2 from the tissue to the lungs anemia deficiency in RBCs quantity of Hgb and hematocrit volume of packed RBCs Causes Blood loss chronic hemorrhage bleeding duodenal ulcer colorectal cancer liver disease acute trauma ruptured aortic aneurysm GI bleeding Increased RBC destruction hemolysis sickle cell disease medication incompatible blood trauma Decreased RBC production deficient nutrients iron cobalamin folic acid decreased erythropoietin maker of RBCs in kidneys decreased iron availability Classification morphologic cellular characteristics lab information etiologic underlying cause Manifestations pallor low Hgb low blood flow to the skin jaundice increased concentration of bilirubin pruritus increased skin bile salt concentration increased heart rate amp stroke volume cardiac output maintained Nursing Implementation blood transfusion drug therapy voume replacement dietarylifestyle changes oxygen therapy patient teaching Gerontological complications common in older adults from chronic diseases or nutritional deficiencies Cardiovascular Hypertension systolic gt140 mmHg diastolic gt90 mmHg current use of antihypertensives primary HTN idiopathic secondary HTN underlying HTN Pre hypertension 10 120139 mmHg systolic 8089 mmHg diastolic Management stage 1 Lifestyle modification 65 of antihypertensives would be unnecessary if the pt would start living a healthy lifestyle Drug Therapy Primary action of drugs to treat HTN reduce SVR reduce volume of circulating blood diuretics adrenergic inhibitors direct vasodilators angiotensinconverting enzyme inhibitors angiotensin II receptor blockers calcium channel blockers CAD coronary artery disease amp ACS acute coronary syndrome atherosclerosis thickening of artery walls causes cholesterol and lipid deposit in artery wall endothelial injuryinflammation result of tobacco hyperlipidemia hypertension diabetes Pathophysiology fatty streak gt fibrous plaque gt complicated lesion modifiable risk factors total cholesterol gt200 trigyceride gt150 HDL lt4050 goal gt60 LDL gt150 goal lt1 00 the usual HTN tobacco EHOH obesity diabetes metabolic syndrome Angina chest pain 11 ischemia compromised blood flow to the heart if left ischemic tissue necrosis will occur Chronic stable intermittent that occurs with the same pattern duration and intensity 515 minute duration rest helps meds can control it Unstable new onset rest doesn t help worsening pattern unpredictable medical emergency Ml heart attack result of maintained ischemia gt20 minutes causing myocardial necrosis 8090 secondary to thrombus loss of contractile function Manifestations SNS stimulation peripheral BV vasoconstriction diaphoresis skin ashen clammy cool Cardio initial BP and HR elevation later BP may drop due to decreased cardiac output Nausea vomiting fever dizziness SOB Care immediate relief vasodilators nitroglycerin VS Q15minutes ECG semifowler s pain assessment houry urine Output oxygen labs relieve anxiety morphine Serum cardiac markers released into blood from necrotic myocardial tissue myoglobin troponin present up to 14 days after MI CKMG Drug therapy nitroglycerine vasodilator reduces pain improves blood flow watch for hypotension morphine pain decreased cardiac workload vasodilator reduces anxietyfear monitor for bradypnea and hypoxia heparin prevents clots from worsening or forming monitor for bleeding aPTT betablockers decrease contractility HR SVR BP reduced reinfarction risk in 1st 24 hours ACE inhibitors prevents ventricular remodeling Cholesterol lowering drugs antiplatelet therapy aspirin calcium channel blockers Complications dysrhythmias 80 of patients heart failure the 1 cause of hospital admission in people over 65 cardiogenic shock Heart Failure abnormal condition involving impaired cardiac pumpingfilling heart is unable to produce adequate CO to meet metabolic needs or systemic circulation demands decreased exercise tolerance Types of Heart Failure Most common left sided from left ventricular dysfunction symptoms backup of blood in L atrium and pulmonary veins pulmonary congestion pulmonary edema right sided from left sided backup of blood in the right atrium symptoms jugular venous distention hepatomegaly splenomegaly vascular congestion of GI tract peripheral edema Clinical manifestations fatigue tachycardia dyspnea orthopnea dry cough unrelieved with cough suppressants dependent edema sudden weight gain of gt3 lb in 2 days nausea A fib Complications high risk fatal dysrhythmias hepatomegaly swelling of liver fibrosis amp cirrhosis can develop over time renal insufficiency or failure Management high fowler s supplemental oxygen continuous ECG decreased IV volume Drugs diuretics beta blockers ACE inhibitors vasodilators digitalis potassium supplements Nutritional Therapy DASH diet sodium restricted daily weight Peripheral Artery Disease of the LE progressive narrowing and degeneration of arteries of neck abdomen and extremities atherosclerosis leading cause usual risk factors Manifestations SS ischemic muscle ace or pain precipitated by exercise but resolves within 1o minutes of rest parasthesia numbness or tingling in toesfeet produces loss of pressure and deep pain thin shiny taut skin 15 loss of hair on lower legs diminished pedal poplital or femoral pulses pallor of foot with leg elevation reactive hyperemia of food pain at rest Drugs antiplatelets aspirin plavix Pneumonia amp COPD pneumonia acute lung inflammation caused by a microbial organism defensive mechanisms of the airway are incompetent or overwhelmed organisms reach the lungs by aspiration from nasopharynx or oropharynx inhalation of microbes present in the air hematogeneous spread from primary infection elsewhere in the body types community acquired lower respiratory tract infection with onset in the community or within 2 days of hospital admission healthcare associated hospital acquired after 2 days of hospitalization ventilator associated after 2 days of mechanical ventilation manifestations feverchills SOB product cough pleuritic chest pain pulmonary consolidation bronchial breath sounds rhonchi crackles fremitus dullness to percussion if fluid is there collaborative care antibiotic therapy oxygen increased fluid intake increased caloric intake balance activityrest antipyretics analgesics 16 medications antibiotic regimen based on type known risk factors severity onset beware of MDR interventions monitor pulse ox specimen collection asepsis reposition q2h adequate activity elevate HOB incentive spirometry aspiration precautions hydrationnutrition oral hygiene vaccine indicated for those at risk 65 years or older 264 years with long term health problemimmunosuppression 1964 who smoke or have asthma live in nursing homes or SNFLTCs evaluation effective respiratory rate rhythm and depth of respirations lungs CTAB pain control SpO2 gt or equal to 95 free of adventitious breath sounds clear sputum from airway COPD 4th leading cause of death kills more than 120k Americansyear airflow limitation not fully reversible abnormal inflammatory response of the lungs combination of chronic bronchitis and emphysema Risk factors cigarette smoking 8090 dust chemicals air pollution infection hereditary aging Patho primary process is inflammation inhalation of noxious particles mediators released caused damaged lung tissue parenchyma destroyed graded as mild moderate severe Manifestations develops slowly chronic cough sputum production dyspnea characteristically underweight with inadequate caloric intake prolonged expiratory phase wheezes increased anterior posterior diameter bluishred colored skin Diagnostics Pl l39s pulmonary function tests chest xray ABG low paO2 increased paCO2 decreased pH increased bicarbonate level found in late stages of COPD Interventions no smoking avoid exposure to pollutants early diagnosistreatment of RTI acute intervention oxygenation positioning balanced activityrest nutritional support DrugNutritional Therapy bronchodilators increase lung volume O2 therapy maintain paO2 reduce cardiac workload rest 30 minutes before eating bronchodilators before meals highcalorie high protein diet is recommended intake 3L of liquidday Outcomes normal breath sounds effective coughing return PaO2 to normal range maintenance of normal body weight


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