NURSE-UN 240 AE1- Exam 2 Week 5 Latest updated 2022,100% CORRECT

NURSE-UN 240 AE1- Exam 2 Week 5 Latest updated 2022 • Fluid regulation important in maintaining homeostasis o Influenced by various body systems ▪ Cardiac ▪ GI ▪ Pulmonary ▪ Pituitary ▪ Renal • Fluid compartments o Extracellular – 1/3 ▪ Interstitial, intravascular o Intracellular – 2/3 • Hydrostatic = pushing force o Osmotic = pulling force • Edema – accumulation of or excess fluid in interstitial space o Develops with changes in normal hydrostatic pressure differences • Average daily fluid intake  mL • Abnormal fluid output – vomiting, wound drainage, hemorrhage • Aldosterone – secreted by adrenal cortex when extracellular sodium levels are low o Prevents both water and sodium loss  nephrons reabsorb them form urine • ADH (vasopressin) – secreted by posterior pituitary in response to changes in blood osmolarity o Water is returned to blood circulation, decreased water secretion • Natriuretic peptides (ANP) – secreted by cells lining atria and ventricles of heart in response to stretch of heart tissue due to increased blood volume and BP o Filtration increased to produce more urine • RAAS o Renin released by kidneys due to decreased BV going to kidneys  converts angiotensinogen (from liver) to angiotensin 1  ACE (secreted by lungs) converts it to angiotensin 2  leads to ▪ Vasoconstriction  increase BP ▪ Aldosterone secretion  increases sodium and water reabsorption  increase BV and BP ▪ ADH secretion  further increases water reabsorption  increase BV and BP • Weight change of 1 lb = fluid volume change of about 500 mL Electrolyte imbalances • Sodium – 135-145 mmol/L (neurological) o Hyponatremia: ▪ Causes: sodium loss (vomiting, diarrhea, diuretic use) or sodium dilution (inappropriate administration of hypotonic IVF) ▪ Signs and symptoms: • Neurologic issues  sudden onset of acute confusion, increased confusion • Seizures • Neuromuscular changes  general muscle weakness, decreased deep tendon reflex • Cardiovascular  • Dependent on type: o Hypovolemia – signs and symptoms of dehydration o Hypervolemia – signs and symptoms of fluid overload o Hypernatremia: ▪ Causes: increased intake, inappropriate administration of IVFs that contain sodium, corticosteroids, hyperaldosteronism, Cushing syndrome ▪ Signs and symptoms • Short attention span and confusion • Lethargic, drowsy • Skeletal muscle  muscle twitching and irregular muscle contractions • Cardiovascular  impaired cardiac function due to decreased contractility • Potassium – 3.5-5.0 (cardiac) o Control over intracellular osmolarity and volume o Regulate protein synthesis, glucose use and storage o Hypokalemia: ▪ Skeletal muscle weakness, thready and weak pulse o Hyperkalemia: ▪ EKG changes, increase GI motility, parenthesis (pins and needles, tingling) • Calcium – 9.0-11.0 (skeletal) o Stored in bones o Absorption requires active form of vitamin D o Hypocalcemia: ▪ Muscle spasm, positive Trosseau (arm) and Chvostek (face) signs o Hypercalcemia: ▪ Mild – increase heart rate and BP ▪ Severe – depressed cardiac conduction and slowed heart rate • Phosphorus – 2.5-4.5 o Found in bones o Activates vitamins and enzymes, assists in cell growth and metabolism o Plasma levels of calcium and phosphorus  balanced reciprocal relationship o Hypophosphatemia: ▪ Decreased cell membrane excitability o Hyperphosphatemia: ▪ Increased cell membrane excitability • Magnesium – 1.5-2.5 o Critical for skeletal muscle contraction, carbohydrate metabolism, ATP formation, vitamin activation, cell growth o Hypomagnesemia ▪ Increased cell membrane excitability o Hypermagnesemia ▪ Decreased cell membrane excitability • Chloride – 96-106 o Imbalance occurs as result of other electrolyte imbalances ▪ Especially sodium  hyponatremia most like = hypochloremia o Treat underlying electrolyte imbalance or acid-base problem • Older adults are more at risk for electrolyte imbalances o Age-related organ changes o Have less total body water • Lungs excrete carbonic acid o Kidney excrete all other acids • Nursing assessment o Age: very young and old at risk o Environment: excessively hot? o Dietary intake: fluids, salt, foods rich in potassium, calcium, and magnesium o Lifestyle: alcohol intake history o Medications: include over-the-counter (OTC) and herbal, in addition to prescription medications • Anesthesia slows down peristalsis and urine output • Enteral – by mouth • Parenteral – by IV (anything that isnt by mouth) o TPN  total parenteral nutrition o Crytalloids – small enough to pass through membrane o Colloids – too big to do so • Types of IVF solutions – described by tonicity in relation to plasma o Isotonic: 0.9% NaCl (normal saline), lactated ringer’s o Hypotonic: 0.45% NaCl (half normal saline), 0.33% NaCl o Hypertonic: 3% NaCl, Dextrose 10% in water (D10W) ▪ Osmotic diuretic – reduces increased intracranial pressure (cerebral swelling or meningitis) • Not all patients require IV fluids – important to get an IV started in all patients just in case of an emergency where later on will need to push fluids • Select most distal sight of non-dominant hand for insertion (if possible) o Increases potential sites for other IVs if needed • Complications: o Fluid overload – dyspnea, shortness of breath, crackles o Infiltration – leakage of non-vesicant (doesn’t irritate tissue) fluid into extravascular tissue ▪ Edema, cool to touch, blanching at site o Extravasation – leakage of IV fluids or medications into extravascular tissue around infusion site (vesicant – irritates tissues) ▪ Can cause damage to tissues o Phlebitis – inflammation of the vein ▪ Warm sensation, erythema • Peripheral catheters – short term use (fluid restoration after surgery, short- term antibiotic administration) • Central catheters and implanted ports – catheters or infusion ports designed for repeated access to vascular system o Long term use – empty into central vein (bigger vessel) o Ex: PICC lines, triple lumen central catheters o At jugular area not usually permanent – cant go home with them Week 6 • Nociceptive pain – somatic or visceral • Neuropathic pain – no physical evidence of damage o Nerve pain • Painful stimuli often originate in extremities o If pain not transmitted to brain – person feels no pain • Two specific fibers transmit periphery pain o A delta fibers – myelinated  fast conduction o C fibers – unmyelinated • Gate-control theory – allows for non-pharmacological interventions to work (ex: massage, ice, acupuncture) o Other nerve fibers conduct and inhibit/block pain stimuli towards the brain • Body can self modulate pain perception  release of endorphins, endogenous opioids • Patients who cant self-report pain are at highest risk for undertreated pain o Checklist of nonverbal pain indicators (CNPI) o Pain assessment in advanced dementia scale (PA11/4/20AD) • Pain management: o Analgesic agents (pain killers) – first line therapy o Multimodal analgesia (multiple types) – preemptive analgesia (before procedure/pain causing agent) o Multiple routes o Around-the-clock dosing o Patient controlled analgesia (PCA) • Analgesics o Acetaminophen (Tylenol, Abenol, Advil) o NSAIDS ▪ Ibuprofen (Motrin, Novo-Profen) ▪ Naproxen (Naprosyn, Nu-Naprox, Aleeve) ▪ Celecoxib (Celebrex) • Opioid analgesics o Full or mu agonists – morphine, fentanyl, hydromorphone, oxycodone, hydrocodone o Mixed agonists antagonists – butorphanol, nalbuphine o Partial agonists – buprenorphine • Adjuvant medication – not primarily designed to control pain but can be used for analgesic purpose • Side effects of opioids o Constipation o Nausea o Vomiting o Pruritus o Sedation o Respiratory depression (less common, most feared) ▪ Narcan (Naloxone) can reverse effect • Physical dependence – normal response after repeated given doses after days o Quick withdrawal will cause biological symptoms • Tolerance – decrease in effect leading to need increase dose (normal response) • Opioid addiction – chronic neurologic and biologic disease o Impaired control, compulsive use, continued use after no longer needing it • Pseudoaddiction – mistaken diagnosis of addictive disease o Patient asking for more medications after not receiving adequate pain relief • Opioid use in older adults start with low doses and slowly titrate • Sleep is regulated by a sequence of physiological states integrated by CNS activity o Hypothalamus o Reticular activating system (RAS) • Sleep = homeostatic process • Stages of adult sleep cycle o 4 stages of NREM o Sleep cycle lasts 90-100 minutes ▪ REM lasts 60 mins o Sleep goes through stages 1-4 then reversal from 4-2 followed by REM o REM – important for memory consolidation and is period when most vivid dreams occur • Hypothalamus = major sleep control center o Promotes wakefulness and REM through hormones • Purpose of sleep still remains unclear o Physiological and psychological restoration o Maintenance of biological functions o Circadian rhythms ▪ Affected by light, temperature, social activities and work routines • Dreams are important for learning, memory and adaptation to stress • Sleep disorders: o Insomnia – adjustment sleep disorder (acute insomnia) ▪ Inadequate sleep hygiene, behavioral insomnia of childhood, insomnia caused by medical condition ▪ Difficulty falling asleep and staying asleep  overall disappointment of quantity and quality of sleep o Sleep apnea – primary central sleep apnea, central sleep apnea caused by medical condition, obstructive sleep apnea syndromes ▪ Daytime sleepiness, loud snoring, wake up feeling unrested o Narcolepsy – cataplexy (brief and sudden loss of voluntary muscle tone triggered by strong emotions), sleep paralysis ▪ Dysfunction in sleep and wake cycle ▪ Not cured but can have medication ▪ Go into REM within 15 mins o Sleep deprivation – emotional distress, medications, environmental disturbances o Parasomnias – somnambulism (sleep walking), night terrors, nightmares, nocturnal enuresis (bed-wetting), body rocking, bruxism (grinding teeth) • Factors influencing sleep o Drugs and substances – hypnotics, diuretics, narcotics, antidepressants, alcohol, caffeine, beta-blockers, anticonvulsants o Lifestyle – work schedule, social activities, routines o Usual sleep patters – may be disrupted by social activities or work schedule o Environment – noise, routines, good ventilation ▪ Not sleeping with someone that you’re used to sleeping with o Emotional stress – worries, physical health, death, losses o Exercise and fatigue – moderate exercise and fatigue can cause a restful sleep o Food and calorie intake – time of day, caffeine, nicotine, alcohol ▪ Glucose increase (surge)  insulin rushes in cell and lowers blood glucose which causes being sleeping after big meal or lots of candy ▪ Full meal before bed time interrupts sleep – GI upset • Pharmacological approaches to sleep  melatonin, chamomile, non- prescription drugs, valerian • Endorphins released during strenuous exercise will interrupt sleep Week 7 • Ventilation – movement of air in and out of lungs • Perfusion – ability of cardiovascular system to pump oxygenated blood to tissues • Diffusion – exchange of respiratory gasses in alveoli and capillaries • CO = SV x HR o CO  volume of blood pumped each minute o SV  amount of blood pumped each heart beat • Frank’s sterling law/curve – chamber performance dictates volume o Stretch of myocardium in relation to amount of blood in it – determines pressure blood will move on into next chamber • When afterload is increased for too long  cardiac issues (hypertrophy) o CO + SV determined by afterload o SV determined by preload + afterload • Impulses traveling through heart – determine contractions o SA node  AV node  Bundle of His  right + left bundle branches  purkinje fibers • Altered cardiac functioning: o Disturbances in conduction (ex: arrhythmias, dysrhythmias) o Altered cardiac output (ex: heart failure: left sided, right sided, bi- ventricular) o Impaired valvular function (ex: valvular stenosis) o Myocardial ischemia (ex: angina, myocardial infarctions or acute coronary syndrome) • Normal sinus rhythm: depolarization = contraction, repolarization = relaxation o P wave  atrial contraction o PR interval  time between beginning of atrial contraction and ventricular contraction o QRS  ventricular contraction o T wave  ventricular relaxation o QT interval  time between beginning of ventricular contraction and end of ventricular relaxation Relaxation of atria not shown because conduction is so small • Early vs late sings of hypoxia o Early: BP elevated unless patient is in shock o Late: RR decreases, patient is cyanotic • Diagnostic studies: o X-ray o Common blood tests: ▪ CBC/Hemogram ▪ Cardiac enzymes ▪ Serum electrolytes ▪ Cholesterol o Bronchoscopy o Lung CT Scan o O2 Sat o Thoracentesis – insertion of pleural effusion needle in pleural space to remove excess fluid o TB testing o Sputum test o ECG • Normal values for CBC o Hemoglobin (g/dL): Male: 13.5 – 16.5; Female: 12.0 – 15.0 o Hematocrit (%): Male: 41 – 50; Female: 36 – 44 o Red blood cell count (x106 cells/ml): 4.5 – 5.5 o White blood cell count (cells/mL): 4,500 – 11,000 o Platelets (platelets/µL): 150,000 – 400,000 • Cardiac enzymes – cardiac muscles release enzymes when injured o Troponin – elevates as early as 3 hours after myocardial injury ▪ Stays elevated for 7-10 days ▪ I: 0.03ng/mL, T: 0.1ng/mL o Creatine Kinase (CK) – peaks 12-24 hours after chest pain ▪ Male: 55-170units/L, female: 30-135units/L o Myoglobin – early index of damage to myocardium in MI or reinfarction ▪ Increases within 3 hours ▪ 90mcg/L • Patients on diuretic therapy – risk for hypokalemia o Patients on ACE inhibitors – risk for hyperkalemia • Cholesterol normal values: o Fasting cholesterol less than 200 mg/dL o Low-density lipoproteins (LDLs; “bad” cholesterol) 100 mg/dL o Very low–density lipoproteins (VLDLs) 7-32 mg/dl o High-density lipoproteins (HDLs; “good” cholesterol) ▪ Male: 40 mg/dL ▪ Female: 50 mg/dL o Triglycerides ▪ 160 mg/dL • Meter-dose inhalers: deliver controlled does of medication with each compression of canister • Dry powder inhalers: breath-activated delivery of medications • Live, attenuated nasal spray flu vaccine not for older adults • Pneumococcal vaccine – every 5 years for those over 65 o Especially for those living in long term care institutions • Emphysema: o Dyspnea o Minimal cough o Pink skin – still oxygenating and are pink because theyre breathing so fast o Pursed lip breathing o Accessory muscle use o Cachexia o Barrel chest o Decreased breath sounds o Hyperinflation • Chronic bronchitis: o Chronic cough o Purulent sputum o Hemopytosis o Mild dyspnea o Cyanosis (hypoxemia) o Peripheral edema (cor pulmonale) o Crackles/wheezes o Prolonged expiration o Obese • Nicotine acts as stimulants to SNS – increased HR, peripheral vasoconstriction, increased BP and cardiac workload o Decreased ciliary activity o Mucous production o Increased difficulty in clearing secretions • COPD patients may appear thin or have unplanned weight loss – use of nutrient stores to breathe • Alpha-1 AntiTrypsin deficiency – allows proteolytic enzymes to deteriorate alveoli o Enzyme gets rid of proteolytic enzymes surrounding alveoli Week 8 • Diabetes mellitus – group of metabolic diseases characterized by hyperglycemia resulting from abnormal insulin production, impaired insulin use or both o Involves improper metabolism of carbs, fats and proteins • Chronic hyperglycemia associated with long-term damage, dysfunction and failure of various organs o Eyes, kidneys, nerves, heart and blood vessels • Gestational diabetes – body cant make enough insulin and use it less effectively (insulin resistance) o Around 24 weeks • Type 1  antibodies present for months to years before symptoms occur and manifestations develop when pancreas can no longer produce insulin – then rapid onset with ketoacidosis o Age: any age but more common in young people o Type: abrupt onset but may have been present for many years o Prevalence: 5-10% o Environmental factors: virus, toxins o Primary defect: absent of minimal insulin production o Islet cell antibodies: present at onset ▪ Autoimmune/ genetic condition: patient will develop antibodies to insulin producing cells Kasoki virus and mumps are associated with it • Type 2  hyperglycemia may go many years without being detected, many times discovered with routine laboratory testing o Age: adults, incidence increasing in children o Type: insidious o Prevalence: 90-95% o Environmental factors: obesity, lack of exercise o Primary defect: insulin resistance, decreased production, altered adopokines o Islet cell antibodies: absent • Metabolic syndrome increases risk for type 2 diabetes  3/5 risk factors indicates metabolic syndrome o Elevated glucose levels o Abdominal obesity o Elevated BP o High levels of triglycerides o Decreased levels of HDLs • Type 1 clinical manifestations: o Weight loss – loss of calories and water in urine o Polydipsia o Polyuria o Polyphagia • Type 2 clinical manifestations: can also present with 3 Ps o Non-specific symptoms o Fatigue o Recurrent infections o Prolonged wound healing o Visual changes • Criteria for diagnosis – to actually diagnose need to repeat test and confirm diagnosis o Fasting plasma glucose ≥ 126 mg/dL ▪ Fasting = no caloric intake for ≥ 8 hours o 2-hr PG ≥ 200 mg/dL during OGTT (75g) ▪ Using glucose load containing equivalent of 75g anhydrous glucose dissolved in water o A1C ≥ 6.5% ▪ Reflects past 60-90 days ▪ Normal: reduces risk of retinopathy, neuropathy, and nephropathy o Random PG ≥ 200 mg/dL ▪ In individuals with symptoms of hyperglycemia or hyperglycemic crisis • Pre-diabetes: FPG 100-125 mg/dL o Known as impaired glucose tolerance or impaired fasting glucose o 2 hour PG higher than normal (140-199 mg/dL) o A1C – 5.7-6.4% o If no preventative measures taken – can develop within 10 years ▪ Leads to microvascular and macrovascular changes • Hypoglycemia (BG ≤ 70 mg/dL) o Causes ▪ Receiving too much insulin ▪ Decreased food intake ▪ Exercise ▪ Alcohol intake o Manifestations ▪ Confusion/irritability ▪ Diaphoresis ▪ Tremors ▪ Hunger ▪ Weakness and visual disturbances ▪ Can mimic intoxication ▪ Untreated can progress loss of consciousness, seizures, coma, and death o Treatment: rule of 15 (if alert to swallow) ▪ 15-20 grams of simple carbs ▪ Recheck BG 15 minutes after treatment ▪ Repeat until BG is above 70 ▪ Patient should eat regularly scheduled meal/snack to prevent rebound hypoglycemia ▪ Check BG again 45-60 minutes after treatment o Treatment: severe  BG ≤ 20 or no improvement after 2-3 doses of simple carbs or not alert enough to swallow ▪ Administer 1 mg of glucagon IM or subcutaneously • Aids in producing/stimulating hepatic glucose production  increases BG levels • Side effect: rebound hyperglycemia ▪ 50% dextrose IV push ▪ Have patient ingest complex carb after recovery • Hyperglycemia (BG ≥ 200 mg/dL) o Causes ▪ Stress ▪ Medications (steroids) ▪ Not taking insulin ▪ Extra sugar intake o Complications: ▪ Type 1: Diabetic Ketoacidosis (DKA)  BG ≥ 250 mg/dL metabolic acidotic state • Positive ketones in blood and urine • Kussmaul’s respirations • “Fruity” breath • Nausea and abdominal pain • Clinical manifestations of dehydration • Treatment: ensure patent airway, administer O2, establish IV access and begin fluid resuscitation, protect from cerebral edema, monitor for fluid overload ▪ Type 2: Hyperglycemic hyperosmolar state (HHS)  BG ≥ 600 mg/dL • Negative ketones in blood and urine • Neurologic symptoms • Clinical manifestations of dehydration • Treatment: IV insulin and NaCl infusions, fluid replacement, monitor!!!, correct underlying precipitating cause o Treatments: ▪ Get medical care ▪ Continue diabetes med as prescribed ▪ Check BG and urine ketones ▪ Drink fluids hourly ▪ Contact HCP with ketonuria • Chronic complications: o Retinopathy o Nephropathy ▪ Males may have erectile dysfunction ▪ Sexual dysfunction o Neuropathy (foot and lower extremities) ▪ Nervous system disease, amputations, pressure injuries (foot), delayed wound healing  call HCP if injury doesn’t begin to heal after 2 days o Cardiovascular disease ▪ Heart disease, high BP, o Complications of pregnancy o Dental disease • Nutritional therapy o Carbohydrates ▪ Minimum of 130 g/day ▪ Fruits, vegetables, whole grains, legumes, low-fat milk ▪ Monitor with CHO counting, exchanges, or experienced-based estimation ▪ Use glycemic index ▪ Sucrose-containing food substituted for other CHOs o Fats ▪ Limit saturated fats to less than 7% of total calories ▪ Limit cholesterol to less than 200 mg/day ▪ Minimize trans fat • Pharmacology o Type 1 – insulin o Type 2 – oral agents (many different classes) and may progress to insulin at some point • Basal-bolus regimen o Intensive or physiologic insulin therapy – most closely mimics endogenous insulin production o Administer multiple daily injections (or insulin pump) with frequent self monitoring of BG (or continuous glucose monitoring system) o Bolus – rapid or short acting insulin before meals o Basal – intermediate or long acting insulin once or twice a day o Goal: achieve glucose level as close to normal as possible as much of the time as possible