Semester 3 Coronary Artery Disease (CAD) PDF

Test 1  Coronary artery disease (CAD) 1. Describe the prevalence of heart disease in Canada....

Test 1  Coronary artery disease (CAD) 1. Describe the prevalence of heart disease in Canada. 2. Describe the etiology and pathophysiology of coronary artery disease, angina and acute coronary syndrome (STEMI and NSTEMI). 3. Identify the modifiable and unmodifiable risk factors for CAD 4. Describe nursing health promotion activities for the control and prevention of CAD 5. Describe the signs and symptoms of coronary artery disease, angina and acute coronary syndrome. 6. Describe the diagnostic tests used in the diagnosis of coronary artery disease and state rationale and nursing management for each. 7. Describe the diagnostic tests used in the diagnosis of angina and myocardial infarction and state rationale and nursing management for each. 8. Describe the pharmacological treatments used for clients with angina and MI 9. Describe the surgical interventions used in the treatment of CAD and MI 10. Describe actual & potential nursing diagnoses in acute and rehabilitation phases of angina or MI. 11. Describe nursing interventions in the acute phase of angina or MI 12. Describe nursing interventions in the rehabilitation of clients following angina and/or MI. Prevalence Etiology Pathophysiology Modifiable & Health promotion S&S Diagnostic tests Pharmacological Surgical Actual & Nsg. Nsg. (Causes) unmodifiable (control & (Rationale & nsg. treatments interventions potential nsg. interventions in interventions in risk factors prevention) management) Diagnoses in acute phase rehab acute & rehab phases CAD + 27.5% of all Hypertension, + A progressive Unmodifiable: + Identify people at P (precipitating + History & + PCI + Activity + rest (semi + sitting (ROM, deaths (2nd tobacco use, type of blood elderly, sex, risk events): physical physical (Percutaneous intolerance r/t ↓ fowlers) ADL’s), progress leading cause) hyperlipidemia, vessel disorder ethnicity, family + Screen for risks: exertion, temp. + CXR coronary coronary blood + administer O2 to walking + Minority, ↓ DM, infections, affecting O2 and history history, lifestyle Extremes, strong + ECG (holter intervention) - flow (bed rest → + take 12 lead + focus on SES, south Asian, toxins, sedentary nutrient flow to the (diet, exercise), emotions, monitor) baloon chair → self care ECG management of: Indigenous life, obesity myocardium Modifiable: health beliefs, stimulants, heavy + Labs (lipid angiogaphy with → ambulation → + insert 2 IV pain, anxiety, (likely have DM + Endothelial + hypertension education, work meds profile) stent stairs); avoid more catheters dysrhytmias, & CAD) injury & = meds, diets, environment, Q (quality): + CABG than 20 beats/ min + continuous ECG complications + women: age of inflammation d/t exercise cardiovascular pressure or ache, (coronary artery above resting rate monitoring deposits → + serum lipids = symptoms choking, bypass graft) osclerosis meds + Risk suffocating, + TMR lateral + Abd. obesity management of heavy, squeezing (transmyocardial lation: form = weight loss causes R (radiation): laser branches of + Tobacco use midsternal, L revascularization) arteries when & physical shoulder & arm, - high energy laser ain is inactivity neck, epigastric to create channels ed → might S (severity): in heart pain d/t Contributing: usually 3-5 mins amount of DM, ↑ blood T (timing): pain flow glucose, at rest → might be depression ACS versible + ECG ardial + exercise stress mia test rmittent + coronary period angina angiography same onset, + echocardiogram on & symp. + nuclear imaging sity pattern + CXR + new onset, at + ECG + Nitrates rest or sleep, + serum level of + LMWH or IV worsening pattern cardiac markers heparin and unpredictable + coronary + Aspirin &/or + ↑ frequency angiography palvix + fatigue (#1 C/I: inability of pt + Morphine for symp.), SOB, to cooperate pain/ anxiety indigestion, during test, + ß-blocker/ ACE anxiety pregnancy, iodine inhibitor allergy, pregancy, + angiography tained + severe pain = renal disorders, intervention/ clot mia → not relieved by propensity for busters/ CABG rsible rest, position bleeding ardial cell change or nitrate Post nsg. Manag.: Fibrinolytic (20 mins) + Ex. of quality monitor VS, agents (clot sequences above pressure on busters) nds on + Loc. = vascular access Action: activate mbus location substernal, site, bed rest for 4 plasminogen to retrosternal, - 8 hrs, extremities dissolve clot mplete epigastric, neck, extended & Outcome: sion of major jaw, arms or back immobilized, reperfuse → full + clammy, ashen, signs of myocardium nes damage to cool to touch skin hematoma, weak + TPA (tissues muscle + ↑ BP & HR, pulse plasminogen nausea/ vomiting, activator) - 60 to fever 90 mins activation + Complications: time dysrhythmias, HF, + TNK  er to have cardiogenic shock, (tenecteplase) han STEMI pericarditis, mplete dressler’s sion of minor syndrome ary artery (pericarditis) or partial + Elderly: sion of major confusion, SOB, dizziness, tial thickness pulmonary edema ge to heart le betic Atypical symp. pathy Like dyspnea ing nerves of be seen on using holter toring  Stress management 1. Recall stress and the physiological response to stress. 2. Recall causes affecting a person’s cognitive appraisal of stress. 3. Describe signs and symptoms of stress. 4. Discuss different types of stressors. 5. Analyze and describe one’s own physiological and psychological reactions to stress. 6. Recognize the link between physiological stress response and pharmacological interventions. 7. Discuss factors that may influence stress tolerance level. 8. Describe causes that may contribute to stress in the nursing profession. 9. Describe nursing interventions for a patient experiencing stress. 10. Describe elements of a stress management plan and how it could be used in a professional situation to reduce stress. Stress & Physiological A physiological response of the body coping to attain homeostasis in the presence of a threatening response situation Causes (General & GENERAL nursing) External: family, work, economics, school, major life changes, loss, etc. Internal: pain, worry, fear, uncertainty, attitudes, etc. (can be worsened by RUMINATION → think back on a stressful situation in the past & worsening the present state) NURSING External: due dates, clinical, exams, etc. Internal: unsure of future, feeling unprepared, etc. S&S Cognitive: ↓ concentration, memory, worry Behavioural: Irritability, withdrawal, violence, less patience Emotional: fear, anxiety, depression, fatigue, anger Physiological: ↑ BP, HR, RR, diaphoresis, constipation, diarrhea, nausea, angina, loss of sexual drive, ↓ immune Types of stressors Physiological: acute or chronic illnesses, pain, insomnia, trauma or injury Psychological: medical diagnosis, failing an exam, family or financial issues, etc. (anything perceived as a threat to survival or to self-image) Daily hassles: getting to metro on time, following up with notes correctly, etc. (frequency and intensity of daily hassles related more to somatic events than life events) Life events Expected (normative): transition to college, marriage, retirement Unexpected (non-normative): miscarriage, death of a child, losing a job, etc. Eustress: stress associated with positive events (help focus, motivate, concentration, etc.) Physiological & GAS (general adaptation syndrome): alarm reaction (when perceived physical or mental stress, psychological fight or flight response gets activated, hence ↑ SNS activity) → Stage of resistance (mobilizing reactions physical resources like fighting back/problem solving with few overt S & S, trying to adapt thru. Allostasis) → Stage of exhaustion (all energy has been used, have minimal S & S, ↓ functions, may result in illness or death, required external resources like meds, psychotherapy)  + Nervous, endocrine and immune systems are the ones responsible for physiological response but might affect other systems + limbic system responsible for stimulating behaviours to cope with the perceived stressor (survival) + reticular formation stimulates RAS producing emotional response to cause insomnia + Hypothalamus signals to release epi & norepinephrine (activate SNS) Link physiological + Heart (↑ HR) → morphine, Dilaudid, Versat response to + Blood vessels (peripheral vasoconstriction) → ↑ BP → metoprolol, thiazide diuretics pharmacological + Lungs (↑ RR, shallow breathing) → Narcotics interventions + Liver (Glycogenolysis) → ↑ glucose → insulin, oral hypoglycemics + GI (↓ secretions, peristalsis) → stimulant laxatives Influencing factors of Internal influences: Biology & genetic endowment, personal characteristics, resilience, coping, sense tolerance level of coherence (comprehensibility, manageability) External influences: Employment & working conditions, strong social support, culture (religion, ethnicity) Response to stressors influenced by factors: intensity (challenge, commitment & taking control), scope, duration, past exposure, no. & nature Response to stressors influenced by characteristics: age, gender, perception of personal control, social support availability, feeling of competence Nsg. interventions + Relaxation coping techniques, support, resource allocation + Encourage talking about the stressor + Health promotion, health teaching, stress management techniques + Aim pt to restore a sense of control Manag. Plan + Relaxation strategies: thought stopping (recognizing & breaking the cycle of negative thought), humor, yoga, music, rhythmic breathing + healthy lifestyle behaviours  COPD 1. Define Chronic Obstructive Pulmonary Disease (COPD). 2. Identify epidemiological factors related to COPD. 3. Understand the pathophysiology underlying COPD. 4. Recognize the risk factors commonly associated with COPD. 5. Recognize the signs and symptoms associated with COPD. 6. Explain the diagnostic tests used in the diagnosis and treatment of COPD. 7. Understand the medical complications associated with COPD. 8. Carry-out the pharmacological treatments commonly used in the treatment of COPD. 9. Identify nursing adaptation problems commonly seen in clients with COPD. 10.Describe nursing interventions for a client in the chronic and acute phases of COPD. 11.Describe the nurse’s role in health promotion related to COPD. COPD A group of lung diseases characterized by chronic inflammation of the airways, bronchioles, and alveoli, which makes breathing difficult. Epidemiological Main cause: SMOKING!!! factors (causes) + environmental exposures (biomass fuel, air pollution, occupational chemicals) + host factors (𝝰1-Antitrypsin (AAT) deficiency) + infection (aggravation of symptoms → mostly common) + Aging (changes in lung structure & resp. muscles) → ↓ expansion d/t alveoli and ribcage stiffness r/t osteoporosis → more susceptible for infection Pathophysiology A group of diseases (emphysema, chronic bronchitis) that impedes a person capacity to fully breath (airflow blockage, impaired gas exchange) Emphysema: pressure limitation in bronchioles; when alveoli is hyperinflated → BRONCHIOLES COLLAPSE → ↓ surface area for O2/CO2 diffusion Chronic bronchi inflammation: chronic inflammation; presence of chronic productive cough for 3 mnths in 2 successive yrs Risk factors + Age + Medical history (impaired cardiovascular, respiratory system) + Smoking S&S + cough, dyspnea + weight loss, fatigue & anorexia + Wheezing, ↓ breath sounds, Adventitious sounds (crackles, Rhonchi - if sputum cleared after coughing) + tripod position + purse - lips on expiration (prevent bronchioles from collapsing) + use of accessory muscles & Barrel chest (top lobes of lungs inflated & lower appear straight) + Polycythemia (↑ RBCs → to compensate the lack of O2 → ↑ hematocrit, hemoglobin) & cyanosis Diagnostic tests + spirometry - breath into a tube through only lips with a blocked nose to observe full force of exhalation + Chest X- ray, CT chest + Arterial blood gas - verifies the amount of gas exchange + Serum 𝞪1-antitrypsin levels (genetic disorder) + sputum culture - to rule out any infection Medical + Pulmonary hypertension: Right ventricle have trouble pumping the hyper viscous blood because of ↑ pressure in lungs complications → hypoxia (constrict circulation to serve vital organs) + Cor pulmonale (R sided HF): crackles, enlarged RV, R jugular vein distension, ascites, weight gain + Pneumonia + Acute resp. failure (Hypoxia or hypercapnia): gas exchange failure; monitor for S&S of hypercapnia (confusion, somnolence, headache, irritability, ↓ in mental acuity, ↑ RR, facial flush, diaphoresis) + ↑ rates of depression (no ADLs), anxiety, panic (not sure what to do) Pharmacological O2 therapy treatments + treats hypoxemia and decreased severity of medical complications + CO2 narcosis: drive to breathe is hypoxemia, increased O2 admin. weakens the drive to breathe + 2L/min, O2 sat around 88-92% (MD orders in TNP/kardex) + Acute respiratory distress = temporary increase O2 airflow and tell Nurse/teacher  + Chest physiotherapy: pulmonary rehab program, progressive exercise plan, pace and activity planning + Resp. therapist: teaching about inspirometer & bronchodilators, breathing exercises, airway clearance techniques (huff coughing), relaxation techniques Nutritional therapy + Smaller meals - less bloating, less pressure on diaphragm → Adequate Ca and vit. D (esp. if on corticosteroids → ↑ bone resorption); less carbs (less CO2) + rest 30 mins prior eating & use of bronchodilators before meals + Fluid intake: 2-3L (fluid & sodium restriction if HF) Beta 2 adrenergics Corticosteroids - anti-inflammatory and enhance b-agonists + Glucocorticoids - decrease inflammation and immunity, influence macro catabolism + Mineralocorticoids - controls H2O volume through aldosterone - Long term usage = altered vascular permeability (edema) and accumulated inflammatory mediators Antibiotics (½ of COPD cases are caused by infection) Nsg. adaptation problems Nsg. interventions + tobacco consumption (clear Qs - Did you smoke in the last year?) + severity of dyspnea: dyspnea scale (palliation & provocation), ADLs activity + frequency & severity of exacerbations + functional assessment (ADLs & IADLs) - physio does it in some places + cough (timing) + hypercapnia (headache, memory loss, ↓ concentration) + Hypoxia (fatigue, insomnia, depression, panic) + edema, ascites, R-JVD (jugular vein distension - tell pt to lay down, turn to left & assess the neck) + anorexia, weight gain, poor appetite Health promotion + prevent disease progression (smoking cessation) + ↓ frequency & severity of exacerbations leading to diseases (Ex. pulmonary HTN) + ↑ exercise tolerance & daily activity + ↑ heath status & quality of life + ↓ risk of mortality  Corticosteroids 1. Understand the rationale for the use of corticosteroids in the treatment of COPD. 2. Identify the most common corticosteroids used in the treatment of COPD. 3. Recognize the most common side effects and adverse effects of corticosteroids. 4. Understand the importance of tapering the dose of corticosteroids. Rationale MOA SE/AE Ind./CInd. Nsg. impliacations Corticosteroids Improve passage of Reduce inflammation Resp. (inhaled): + drug allergies + obtain baseline air in and out of & enhance activity of pharyngeal irritation, + used in caution: physical assessment airway (usually 𝜷-agonists (relax coughing, dry mouth gastritis, GERD, & lab studies used to treat muscles in your lungs Cardio: HF, cardiac ulcers , diabetes + assess for F&E COPD) for easier breathing) edema, HTN (↑ blood glucose) imbalances preventing CNS: convulsions, (hypernatremia, inflammatory headache, vertigo, hypokalemia & fluid processes, “steroid psychosis” retention) accumulation of Endocrine: Cushing’s + Oral forms given imflammatory syndrome (↑ body & with food or milk → mediators & edema; facial hair, moon face, ↓ GI upset mucus production in buffalo hump, easy + clear nasal bronchioles bruising), irregular passages before menstruation, carb administering nasal intolerance, cortico. (Flonase) hyperglycemia + Pt teaching to GI: peptic ulcers, avoid contact with pancreatitis, abd. people having any distention kind of infections Integ.: fragile, + do not take with petechiae, ecchymosis alcohol, ASA or Musculoskeletal: NSAIDs (can cause muscle atrophy, peptic ulcer disease) osteoporosis → from the breakdown of Ca from bones & release in blood Fluticasone Symptom manag., SE: hoarse voice, sore Rinse mouth after Proprionate prevention of throat, cough, dry use (Flovent) - inhaled exacerbations mouth AE: oral candida Methylprenisolone Initial treatment of - IV acute COPD Prednisone - oral Treatment of Taper dose instead PO COPD of stopping abruptly exacerbations - life threatening adrenal crisis Pharmacology Beta2 Adrenergic Anticholinergics Xanthines corticosteroids Agonists MOA Stimulates beta-adrenergic Inhibits Acetylcholine (ACh) Stimulates cAMP production, inhibits glucocorticoid receptors in the airway (s.m.) receptors in order to prevent leading to bronchodilation (s.m.) receptor, inhibiting leading to bronchodilation bronchoconstriction. inflammatory signals (causing Stimulates CNS, leading to COPD) enhanced respiratory drive INH, PO, IV, IM, PR Indications Prevent and treat acute onset Prevents and treats Treats dyspnea, Treats dyspnea, dyspnea, wheezing, coughing, bronchospasms, dyspnea, bronchospasms, wheezing, bronchospasms, wheezing, bronchospasms and chest wheezing and coughing caused coughing and chest tightness coughing caused by: tightness caused by: by: caused by: Asthma Asthma Asthma Asthma COPD/E COPD COPD COPD Prevents asthma attacks Contraindications C/I: allergies, uncontrolled C/I: allergies (including atropine C/I: allergies, uncontrolled C/I: allergy dysrhythmias, stroke risk sulphate) dysrhythmias, seizures, Pre: gastritis, reflux disease, (C/I) or Precautions Pre: palpitations, tachycardia, Pre: acute-angle closure hyperthyroidism, peptic ulcers ulcer disease, DM (causes (Pre) nervousness glaucoma, prostate enlargement Pre: oral contraceptives, increased blood glucose) caffeine, sympathomimetics, Overuse of non-specific high-carb low-protein diets = Pharmacology Beta2 Adrenergic Anticholinergics Xanthines corticosteroids Agonists adrenergic agonists (beta and decreased theophylline alpha receptors) may lead to excretion (xanthines anxiety, palpitations, tremor and metabolised to theophylline) heightened HR Side Effects CV: hypo/hyper-tension, CV: tachycardia, palpitations CV: tachycardia, extrasystole, Resp: irritation, coughing, tachycardia Neuro: excitation, palpitations, dysrhythmias xerostomia, Endo: hyperglycemia disorientation, hallucinations, GI: nausea, vomiting, anorexia, CV: Neuro: vascular headache drowsiness, confusion, anxiety, acid reflux CNS: Resp: paradoxical headache Urin: high urination, MS: osteoporosis bronchospasm GI: xerostomia, distress hyperglycemia Endocrine: Adrenal (bronchoconstriction after Resp: less bronch. and nasal insufficiency (esp. if med is administering bronchodilator) secretions, coughing suddenly discontinued) Musc: tremors Urin: urinary retention Integ: thinned skin, Gland: less sweating Sens: dilated pupils (blurred), high ocular P Drug Interactions Adrenergic-blockers + Anticholinergic + Enhancers: caffeine, Alcohol B-agonists = reduced anticholinergic = beta-adrenergic agonists ASA effect of B-agonist inhibit other drug Diminishers: antibiotics, herbal NSAIDs B-agonists + MAOI absorption supplements, cigarettes, antidepressants and high-carb low-protein diets similar drugs = high risk of hypertension B-antagonist + Antihyperglycemic drugs = less effective anti hyperglycemia (especially epinephrine) Diabetes Mellitus 1 1. Describe diabetes as a major health problem in the population. 2. Describe the risk factors for diabetes. 3. Recognize epidemiological factors related to diabetes. 4. Describe the three cardinal symptoms of diabetes. 5. Relate the cardinal symptoms to the underlying pathology. 6. Compare and contrast Type 1 and Type 2 diabetes. 7. Identify the most common diagnostic tests used in the diagnosis and management of diabetes. 8. Describe the acute complications of diabetes and their respective management. 9. Illustrate understanding of a standard hypoglycemic protocol. 10. Describe the three major treatment modalities used to treat diabetes (diet, exercise, medications). 11. Identify the main drug classifications used in the therapeutic control of diabetes (insulin and oral). 12. Describe short- and long-term nursing goals in the management of a client with diabetes.  Diabetes 1 Description + Abnormal insulin production made by the 𝞫-cells of pancreas and/or impaired insulin utilization + DM is the major cause of: blindness, kidney failure, heart attacks, stroke, lower limb amputation + medical costs of a person with DM is 3 to 4 times higher Risk factors + Indigenous: 3 to 5 times more likely → eat more canned food and sugary foods d/t the location + Predisposition (Family/Gestational DM) + Diet (high in sugar) + Sedentary lifestyle + Age (45+) + Obesity → visceral fat (belly) + HTN, DLP + Vascular disease + Polycystic ovarian syndrome (PCOS) Epidemiological + corticosteroids factors (causes) + emotional, physical stress + Genes + Hormonal imbalances + Lifestyle (first, exercise) Cardinal symptoms + Polydipsia (excessive thirst) → (↑ blood glucose causes polyuria in effort to eliminate excess glucose → loss of fluid stimulates thirst) + polyphagia (excessive hunger) → (body's inability to burn glucose for fuel due to the lack of insulin or insulin resistance → hunger) + polyuria Comparison btw. Type 1 (Juvenile diabetes) Type 1 and 2 diabetes + chronic, people have glucose monitors as children & become normal when they get used to it + 𝞫-cells of pancreas are destroyed by immune system + S & S: major weight loss + Age of onset: rapid, before 30, usually acute: 11-13 years + Etiology: virus, toxins (autoimmune process in susceptible) + Treatment: meds → insulin Type 2 + more of a lifestyle change + not enough insulin is released + S & S: weight gain or weight loss + Age of onset: 45 yrs + Etiology: lifestyle habits (sedentary life, obese), belly fat, history + Treatment: meds (PO, common - ozempic), weight gain, diet, exercise Diagnostic tests + fasting or normal plasma glucose level + 2HR OGTT (oral glucose tolerance test) level: no food 8-12 hrs before test, drink glucose and take test + glycosylated hemoglobin (HBA1c): ↑ amounts of HBA1c in RBCs of DM patients Hypoglycemic + immediate ingestion of 15-20 g of simple carbs, another 15-20 g in 15 mins if no relief obtained (Orange protocol juice, 6-8 lifesavers)  + follow-up with snack (Peanut Butter sandwich, cheese and crackers) if the next meal is 1hr+ away + discuss with MD about insulin or OHA dosage Acute & chronic Hyperglycemia complications S&S: Polyuria, Polyphagia, polydipsia, Weakness, fatigue, Blurred vision, Headache, N&V, Progression to DKA or HHS Causes: Too much/little food, emotional stress, corticosteroids, stress Hypoglycemia S&S: Glucose under 4mmol/L, Numbness in extremities, Rapid HR, emotional changes, nervousness, slurred speech, seizures, unsteady gait Causes: Alcohol, too little food, too many diabetic meds Macrovascular: atherosclerotic plaque development, cerebrovascular injury, cardiovascular disease Microvascular: retinopathy, nephropathy, neuropathy Major treatment + Diet modalities Type 1: no food restrictions Type 2: limit sugar and fats, increase fibre and H2O consumption, control lipid and glucose intake, control BP - WEIGHT LOSS + Exercise - increase insulin sensitivity, decrease BP, promotes circulation + Medication Drug classifications ST & LT goals + promote well-being + reduce symptoms + prevent acute complications of hyperglycemia & hypoglycemia + delay onset & progression of long-term complications Oral & IV anticoagulants in management of PE & A-fib 1. Describe Pulmonary Embolism (PE) 2. Describe Atrial Fibrillation (AF) 3. Identify the signs and symptoms of Pulmonary embolism and Atrial fibrillation 4. Identify risk factors for PE and A-fib. 5. Describe diagnostic tests used in PE and A-fib. 6. Identify the pharmacological interventions in PE and A-fib. (Heparin, Warfarin, Novel anticoagulants) 7. Describe the contraindications, adverse effects and interactions seen with IV heparin 8. Describe the lab tests needed to monitor the effectiveness of Warfarin and IV heparin. 9. Understand the concept of bridging. 10. Describe nursing care and collaborative care of a client in hospital with PE and A fib  11. Describe pertinent client teaching for a patient who is being discharged on an anticoagulant Pulmonary embolism (PE) Atrial fibrillation (A.fib) Description Blocked pulmonary arteries by a dislodged emboli An electrical misconduction in the atrium → loss of (cause could be the embolus formed during A.fib → effective atrial contraction stroke or PE; or r/t DVT) + most common dysrhythmia + obstructs perfusion of alveoli and could also lead to + Ectopic foci (abnormal pacemaker sites outside SAN) HF → blood pools up in atrium (risk for thrombi & + lower lung lobes are commonly affected r/t higher embolus traveling to brain) and starts to quiver → ↓ CO blood flow + ↑ risk of stroke & PE with A.Fib + Venous thrombo-embolism (VTE): umbrella term for DVTs, emboli, thrombi S&S + most have no leg symptoms + Atrial rate upto 600bpm + tachypnea + ventricular rate 50 - 180 bpm, irregular rhythm + crackles, rhonchi + palpitations + tachycardia + fatigue + classic triad: + SOB (on exertion) - Dyspnea + chest discomfort - chest pain (inflammatory response of PE) + dizziness or light - headedness - Hemoptysis (coughing up blood) + sweating + hypotension + feeling anxious + pallor + hypoxemia + pleuritic chest pain + slight fever + productive cough with blood streaked sputum Example V/S: RR: 25 (hyperventilation) BP: low HR: > 120 (overcompensating) T: 38 C O2: < 89 % Causes / Risk + fat emboli (fractured long bones) + Age (> 80) factors + air emboli (improper administration of IV therapy) + HTN + bacterial vegetations + damage to heart valves: rheumatic heart disease + amniotic fluid + CAD → MI + tumours + HF + malignancy (tumour → cancerous) + cardiomyopathy + surgery (orthopedic) + pericarditis or myocarditis + hospitalization Can be associated with: + long duration air travel + Diabetes + hormone use or pregnancy + Hyperthyroidism (overactive thyroid → overconduction) + alcohol intoxication (heavy use) + Cardiac surgery (CABG)  + Caffeine & stress Diagnostic tests + spiral CT scan → most used, IV contrast to view + Physical exam blood vessels + ECG + ventilation-perfusion scan (VQ scan) → assess + Echocardiogram (look for ejection fraction) pulmonary circulation & gas exchange, if pt can’t have + Holter monitor IV contrast + blood tests + D-dimer blood test → amount of cross-linked fibrin + stress test fragments + pulmonary angiography → catheter through antecubital or femora vein to visualize pulmonary vascular circulation + chest X-ray → atelectasis, pleural effusion + echocardiogram → ST-segment, T-wave changes + ABG, aPTT, CBC, INR, Trop, B-tpe natriuretic peptide (BNP) Pharmacological + Anticoag therapy: heparin, LMWH, warfarin, + Rate control: Ca channe blockers (diltiazem) & interventions coumadin, apixaban 𝜷-blockers (metroprolol) + platelet therapy + Rhythm control: antiarrhythmyics (amiodarone, + fibrinolytic agent: tissue plasminogen activator, digoxin) → used for conversion to sinus rhythm as alteplase well) + pulmonary embolectomy (removal of blood clots + Long term anticoagulation therapy: blocking the lungs): threatening situation - Prevent embolic events + inferior vena cava filter - Bridging: - Placed after pulmonary embolectomy and Initial treatment is parenteral (UFH, prevents further emboli LMWH) for 5 days until PO anticoagulant is effectively keeping INR results within desired range for 24 hrs Warfarin requires 2-5 days to take effect, therefore we overlap Heparin and Coumadin to ensure anticoagulant effect Usually added with clopidogrel (plavix) & ASA to reduce major vascular events (stroke) but increases risk of severe hemorrhage INR = [0.8 - 1.2], for anticoag patients [2.0-3.0], PTT = [70-110] Nsg & Prevention Assess collaborative care + sequential compression devices, ambulation + assessment of hemodynamic instability and identify + pt teaching on anticoag therapy to treat underlying cause - Heparin, LMWH, warfarin, coumadin, + symptoms since when, other medica conditions, apixaban, etc family Hx, any other heart disease ot thyroid condition + antiplatelet therapy: ASA, clopidogrel Treatments + monitor V/S, cardiac dysrhythmia, pulse oximetry, Cardioversion: ABGs, lung sounds + electric conduction making heart pump at norma rate  + Labs: aPTT & INR + small electrodes placed to trigger normal rhythm + assess complications of anticoagulant therapy + pt should have had A.fib < 48 hrs ago (bleeding, hematomas, ecchymosis) and PEs (hypoxia, + can cause thrombi and embolus to dislodge hypotension) Catheter ablation: + perform interventions r/t immobility (cause more + pt who can’t be in long term anticoagulation therapy thrombi) & fall precautions (if on anticoags, they might + radiofrequency energy used to burn the scar tissues bleed more than usual after fall) causing tachydysrhythmias Complications + dyspnea + ischemic stroke + pulmonary infarction → alveolar necrosis and + PE hemorrhage → sometimes necrotic tissue might get + cardiogenic shock infected and abscess (a buidup of pus) develops + HF + pleural effusion: accumulation of fluid in the pleural cavity + Pulmonary HTN (recurrent emboli) Client teaching  IV heparin MOA Unfranctioned heparin: antithrombin inhibiting thrombin-meiated conversion of fibrinogen to fibrin through factors 2, 9, 10, 11 & 12; inhibits clotting enzymes & factor Xa SE & AE + Osteoporosis + bleeding (hematuria, epistaxis, ecchymosis, etc) + HIT (heparin induced thrombocytopenia) I & C/I I: used prophylactically (prevention of clot/growing of pre-existing clot), prevents clots associated w/MI, unstable angina, atrial fibrillation, indwelling devices, immobility C/I: acute/risk of bleeding, leukaemia, pregnancy, colitis, GI obstruction, recent surgery Drug interactions Capsicum (bell) pepper, feverfew, garlic, ginger, gingko, ginseng Nsg. implications + monitor aPTT + antidote - protamine + assess for signs of bleeding (hypotension, tachycardia, heamturia, melena, petechiae, etc) +instruct pts to report any type of bleeding (gums, from nose, bloody urine, etc.) + avoid any sudden changes in diet like increase vit K foods (broccoli, spinach, kale, greens) Heart failure and electrolyte imbalance 1. Describe heart failure. 2. Identify the incidence of heart failure in the population. 3. Describe the etiology of heart failure. 4. Identify risk factors that precipitate or exacerbate heart failure. 5. Describe the pathophysiological process related to heart failure. 6. Differentiate between left- and right-sided heart failure and the related signs and symptoms. 7. Differentiate between acute and chronic signs and symptoms in heart failure. 8. Describe the causes that contribute to heart failure. 9. Describe the effects of the electrolytes potassium, sodium and calcium on the normal functioning of the heart. 10. Describe the compensatory mechanisms to manage a failing heart. 11. Describe the diagnostic tests typically ordered in association with heart failure. 12. Describe collaborative treatments used in the control of cardiac failure. 13. Generate nursing diagnoses commonly seen in clients with heart failure. 14. Describe nursing interventions for a client experiencing heart failure. 15. Describe health teaching for a client with chronic heart failure.  Heart Failure Description + impaired cardiac pumping or filling → inadequate CO; CO = HR x SV + Baroreceptors: present in carotid sinuses & aortic arch are sensitive to stretch of pressure; hypothalamus → temporary stopping of SNS & enhancement of PNS → ↓ HR & vasodilation + Chemoreceptors: present in carotid & aortic bodies are sensitive to gas exchange of the body; ↓ CO2 & ↓ plasma pH → resp. Acidosis → ↑BP → ↑ cardiac activity Pathopysiology + inability of heart to pump blood → insufficient oxygen and nutrient delivery to tissues and compensatory mechanisms (like fluid retention and increased heart workload) + a cycle of reduced cardiac output, compensatory mechanisms, and progressive cardiac damage, ultimately leading to congestion, organ dysfunction, and reduced quality of life + normal EF: 55-70% + HF c preserved EF: inability of ventricles to relax & fill during diastole caused by Lt vent hypertrophy from HTN, AS, hypertrophic cardiomyopathy Causes/ risk factors Causes + CAD, HTN + rheumatic heart disease: infection or inflammation of heart or valves + congenital heart disease + pulmonary disease + cardiomyopathy: heart muscle’s inability to pump blood + anemia: ↓ O2, ↓ Hgb + bacterial endocarditis: common heart infection, valvular diseases + acute MI, dysrhythmias, pulmonary embolus + thyrotoxicosis + rupture of papillary muscle + Ventricular septal defect → some babies born with it & hole in septum (divided V & A → O2 & CO2 mix up) + stroke volume: amount of blood pumped out of Lt ventricle/beat + Preload: filling of Rt vent. Before the next contraction - vent. Diastolic dysfunction c vent. Hypertrophy (stiff & thickened) + Afterload: degree of peripheral resistance against which Lt vent. Must pump, pulmonary or systemic pressure - HTN & AVD (aortic valve disease) → heart hypertrophy + cardiac contractility: ability of heart to contract  - SNS release of epi & norepi → ↑ intracellular Ca → Contractility + HR: if ↑HR → ↑ CO coz more blood is being pumped out; but if ↑ HR persists (Ventricular tachy) → ventricles pump at 180 → no time to fill up → contracts often & no systemic circulation Risk factors + age → cardiac muscle hypertrophy + DM → insulin resistance & effect on vent. Remodelling + tobacco use → ↑ pulmonary pressure → exerts a pressure load on RV → Rt vent hypertrophy of tissues + obesity + ↑ serum cholesterol + Infection → ↑ O2 demand of tissues, stimulating ↑ CO Starling’s Law: degree of stretch is directly r/t force of contraction (preload & CO) Complications + ventricular dysfunction + ↓ quality of life + shortened life expectancy + Pleural effusion (good lung down → turn them to unaffected side) + dysrhythmias (A.fib, V.fib & Vtach) + embolic cardiovascular accident + hepatomegaly + renal insufficiency/failure d/t excessive diuretics as well S&S LF (blood back up in Lt atrium & pulmonary veins → ↑ pulmonary pressure) + pulmonary edema: fluid move from vascular space to pulmonary interstitial space (anxious, pale, synoptic, clammy & cold skin, use of acc muscles, adv. Sounds, tachycardia) + ascites + impaired gas exchange + activity intolerance + dyspnea, cyanosis, cough w frothy sputum, orthopnea + ↓ PaO2, ↑ PaCO2 RF (backward flow to Rt atrium & venous circulation + peripheral edema + hepatomegaly, splenomegaly + jugular vein distension + ascites + GI tract congestion → dyspepsia, anorexia, weight loss, cachexia + pleural effusion Effects of electrolytes + sodium: transmission of nerve impulses, muscle contraction; hypernatremia (thirst, dry, sticky mucous membranes, impaired LOC, shock, Cushing's syndrome); hyponatremia (polydipsia, abnormal water retention, tachycardia, N/V, thready pulse, muscle spasm, tremors, coma) + potassium: conduction of nerve & muscle impulses, maintenance of cardiac rhythms; hyperkalemia (abd. Cramping, dysrhythmia, anxiety, paresthesia → kayexalate, diuretics, D50W (prevent hypoglycemia) + Humulin R); hypokalemia (dysrhythmia, ↓ peristalsis, paralytic ileus, malaise, polyuria) + Calcium: transmit nerve impulses, myocardial contractions, blood clotting, teeth & bone formation, muscle contractions; hypercalcemia (depressed reflexes, bone pain, coma, ↓ memory, confusion); hypocalcemia (positive trousseau’s or Chvostek’s sign, laryngeal stridor  + Magnesium: metabolism of protein & carbs, neuromuscular irritability; hypermagnesemia (somnolence, impaired reflexes, bradycardia, hypotension → IV CaCl); hypomagnesemia (hyperactive deep tendon reflexes, tremors, vasodilation, cardiac dysrhythmias) Compensatory Ventricular dilation mechanisms + starling’s law + eventually overstretched muscles can’t contract → ↓ CO Ventricular hypertrophy + ↑ muscle mass & cardiac wall thickness → poor contractility, ↑ O2 demand, inadequate circulation → tissue ischemia, dysrhythmias SNS activation + epi & norepi → ↑ HR, myocardial contractility, peripheral vasoconstriction to have more pressure to blood through + ↑ O2 demand & ↑ workload of failing heart Neurohormonal response + ↓ blood flow to kidneys → RAAS (renin-angiotensin-aldosterone) Diagnostic tests + history & physical exam + chest x-ray → hypertrophy, pleural effusion + ECG - ADHF + BNP or N-terminal pro-BNP → cardiac function + lab studies: CBC, lytes, renal function, urinalysis (hyperosmolar dehydration → K+ , ketones, Na), glucose (↑ glucose → ↓ V. remodelling), thyroid function (affects hormones of metabolism) + echocardiogram → ultra sound of heart (blood flow of chambers, the valves) + cardiac catheterization + cardiopulmonary stress test + MRI, CT scan, endomyocardial biopsy + angiogram Collaborative + high fowler’s position with feet dangling on the side or put feet of the bed at the lowest → ↓ venous return by blood treatments & Nsg. pooling in extremities & ↓ intra-abdominal pressure for better ventilation interventions + supplemental oxygen: give O2 even if sat is at 95% (heart working more d/t decompensated O2) + continuous monitoring + IV diuretics mainly Lasix, spironolactone (SE: gynecomastia → enlarged breasts) + hemodialysis (if c AKI/ acute renal failure)  + IV nitroglycerin: vasodilator → ↓ afterload & ↑ myocardial oxygen supply + Nipride, Morphine IV, Nesitride → ↑ CO & ↓ pulmonary congestion + Noninvasive ventilatory support (BiPAP) → give pressure into pt’s lungs to open up alveoli + devices: cardiac resynchronization therapy, ICD, mechanical circulatory support, cardiac transplantation Nutritional therapy + substitute salt with lemon juice, DASH diet + how to read nutritional labels + fruits & vegetables, eating out → ask for foods low in sodium + fluid restriction (1.5-2L) unless dehydrated Drug therapy + Diuretics + ACE inhibitors (↓ pulmonary artery pressure → RF) + 𝜷-adrenergic blockers (carvedilol & metoprolol) → block the negative effects of SNS + ARBs (Angiotensin 2 receptor blockers) → Valsartan, Losartan + Anticoags (Lovenox - prophylactic, Heparin - therapeutic) Nsg. diagnoses Goals: treat underlying cause & contributing factors, maximize CO, alleviate symptoms, improve ventricular fct., improve quality of life, ↓ preload & ↑ contractility + activity intolerance + fluid volume excess + impaired gas exchange + anxiety + deficient knowledge Health teaching + refer to HF clinic (provide self management coaching - take BP, pulse oximetry, H & S foundation) Oral hypoglycemics 1. Explain the mechanism of action of the different classifications of oral hypoglycemic agents (OHA): insulin secretagogues, biguanides, thiazolidinedione, alpha-glucosidase inhibitors, dipeptidyl-peptidase inhibitors.  2. Describe the indications and contraindications of each classification. 3. Identify the therapeutic and adverse effects of OHAs. 4. Identify the risks of drug interactions. 5. Describe the assessment necessary prior to and after administration of these drugs. 6. Describe how to evaluate the effectiveness of OHAs. 7. Describe pertinent client teaching related to the OHAs. Pharmacology MOA SE Drug interactions Nsg. management Sulphonylureas + ↑ insulin production from + ↓ chance of prolonged + Hypoglycemic effect + Overall concerns: Is pancreas hypoglycemia increases when taken under stress, Has an + Stimulate insulin secretion + Hypoglycemia, with alcohol, anabolic infection, Has an illness from the beta cells of the hematological effects, steroids, many other or trauma, Is pregnant or pancreas nausea, epigastric drugs lactating + Improve sensitivity to fullness, heartburn, many + Adrenergics, + Oral antidiabetic drugs insulin in tissues others corticosteroids, thiazides, - Always check + First generation: others may reduce blood glucose chlorpropamide hypoglycemic effects levels before (Novo-Propamide), + Caution to pts with giving tolbutamide (not used as renal impairment – - Give 30 minutes frequently now) increased risk of before meals + Second generation: hypoglycemia (usually) glimepiride (Amaryl), + Sulfonylureas may - 𝛂-glucosidase gliclazide (Diamicron, interact with alcohol, inhibitors are generic), glyburide (Diabeta, causing a nausea, given with the Euglucon, generic) vomiting, flushing, first bite of each dizziness, throbbing main meal headache, chest and - metformin is abdominal discomfort taken with meals + Insulin (additive to reduce GI effects) effects + 𝜷-Adrenergic blockers + Monitor for therapeutic + Diuretics effects - Decrease in Meglitinides + Stimulates rapid and + Headache, + 𝜷-Adrenergic blockers blood glucose short-acting release of insulin hypoglycemic effects, (Mask symptoms of levels to the level from the pancreas dizziness, weight gain, hypoglycemia, Prolong prescribed by + Taken 30 minutes before joint pain, upper hypoglycemic effects of physician each meal up to time of meal respiratory infection or insulin) - Measure + Should not be taken if meal flulike symptoms + Diuretics (Can hemoglobin A1c skipped potentiate hyperglycemia; to monitor + Examples: Repaglinide exact mechanism of how long-term (GlucoNorm) → shorter thiazide diuretics cause compliance to effect the development of diet and drug Nateglinide (Starlix) hyperglycemia is therapy Pharmacology MOA SE Drug interactions Nsg. management unknown. It is believed to + Overall goals: Active involve worsening of patient participation, Few insulin resistance, or no episodes of acute inhibition of glucose hyperglycemic uptake, and decreased emergencies or insulin release, among hypoglycemia, Maintain other pathways) normal blood glucose levels, Prevent or delay Biguanides + Reduce glucose production + Primarily affects + cimetidine chronic complications, by liver gastrointestinal (GI) tract: (hypoglycemia) Lifestyle adjustments + Enhance insulin sensitivity abdominal bloating, + diuretics, steroids (↑ with minimal stress at tissues nausea, cramping, metformin effects) + Acute intervention: + Increase uptake of glucose diarrhea, feeling of + 𝜷-Adrenergic blockers Stress of illness and by tissues fullness + Contrast media (↓ surgery - ↑ blood glucose + Do not increase insulin + May also cause metallic excretion → lactic level, Continue regular secretion from the pancreas taste, reduced vitamin acidosis) meal plan, ↑ intake of (do not cause hypoglycemia B12 levels → anemia (eat noncaloric fluids, + Do not promote weight dates, fish, meat, poultry, Continue taking oral gain eggs, dairy products) agents and insulin, + Example: Metformin + Can cause lactic Frequent monitoring of (Glucophage) → absorb acidosis, which is rare but blood glucose (Ketone glucose better lethal if it occurs testing of glucose >14 + Does not cause mmol/L) hypoglycemia (directly + Patients undergoing acts on liver & not on surgery or radiological insulin levels) procedures requiring + ↓ hepatic glucose contrast medium should production, ↓ intestinal hold their metformin on glucose absorption day of surgery and to 48 hours → Begun after serum creatinine has been α-Glucosidase + “Starch blockers” + Can cause flatulence, + Insulin (additive checked and is normal inhibitors + Slows down the absorption diarrhea, abdominal pain effects) + Educate on disease of carbohydrates in the small + Do not cause + 𝜷-Adrenergic blockers process, physical activity, intestine hypoglycemia, + Diuretics medications, monitoring + Must be taken with first hyperinsulinemia, or blood glucose, diet, bite of each meals weight gain resources. Enable patient + prevent excessive to become most active postprandial blood glucose participant in his/her care elevations → reduce the impact of carbohydrates on blood sugar + Example: Acarbose (Glucobay) Thiazolidinediones + Most effective in those + May cause moderate with insulin resistance weight gain, edema, mild Pharmacology MOA SE Drug interactions Nsg. management + ↓ insulin resistance → ↑ anemia insulin sensitivity, transport, + May cause hepatic and utilization at target toxicity—monitor liver tissues alanine aminotransferase + ↑ glucose uptake and use in (ALT) levels skeletal muscle Inhibit glucose and triglyceride production in the liver + Inhibits hepatic glucose production + Examples: Pioglitazone (Actos) Rosiglitazone (Avandia) Dipeptidyl + Slows the inactivation of + Potential for peptidase-4 (DDP-4) incretin hormones hypoglycemia nhibitor inhibit glucagon release → ↑ insulin secretion, ↓ gastric emptying, and ↓ blood glucose levels. + Examples: Sitagliptin (Januvia), Saxagliptin (Onglyza) Sodium-Glucose + work by blocking the Cotransporter 2 reabsorption of glucose by SGLT2) Inhibitors the kidney → ↑ glucose excretion + If metformin is contraindicated as first-line treatment, an SGLT2 inhibitor can be considered + Interaction with metformin + Examples: dapagliflozin (Forxiga), empagliflozin (Jardiance) GLP-1 + GLP-1: a physiological glucagon-like hormone that has multiple peptide) receptor actions on glucose agonist + Mimics the action of the GLP-1 hormone: Helps pancreas produce more insulin + ↓ hepatic glucose production reduction of food intake by ↑ Pharmacology MOA SE Drug interactions Nsg. management satiety, delay in gastric emptying thereby reducing caloric intake, lowering appetite, hunger, food craving, and body fat. Example: Ozempic (semaglutide), dulaglutide (Trulicity) Insulins 1. Describe the indications and contraindications of Insulin. 2. Identify the therapeutic and adverse effects of Insulin. 3. Identify the risks of drug interactions. 4. Describe problems that can arise in drug therapy. 5. Describe the assessment necessary prior to and after administration of these drugs. 6. Describe pertinent client teaching related to Insulins. 7. Describe how to evaluate the effectiveness of Insulins. Insulins Metabolic Insulin resistance: Body tissues do not respond to insulin → Insulin receptors are either unresponsive or insufficient abnormalities in number → hyperglycemia Pancreas ↓ ability to produce insulin: β cells fatigued from compensating → β-cell mass lost Inappropriate glucose production from liver Alteration in production of hormones: Play a role in glucose and fat metabolism → Contribute to pathophysiology of type 2 diabetes  Insulins Definition + Function as a substitute for the endogenous hormone + Have same effects as normal endogenous insulin + Restore the diabetic patient’s ability to: Metabolize carbohydrates, fats, and proteins, Store glucose in the liver, Convert glycogen to fat stores + Insulin therapy aims for tight glucose control + To reduce the incidence of long-term complications Rapid - acting analogue Short-acting (clear) Intermediate - acting Extended long-acting (clear) (cloudy) (clear) Info + mimics endogenous + mimics endogenous + NPH (Novolin, Humulin + mimics endogenous insulin insulin N) insulin + lispro (Humalog), aspart + regular (Humulin R) + insulin isophane + glargine (Lantus), detemir (NovRapid), and glulisine + Only insulin that can be + Has a cloudy appearance (Levemir) (Apidra) given IV bolus/infusion + Is slower in onset and has + Injected once a day at + Injected 0 to 15 minutes + Injected 30 to 45 a more prolonged duration bedtime or in the morning before meal minutes before meal than endogenous insulin + Released steadily and + Onset of action 15 + Onset of action 30 to 60 + more vulnerable for continuously minutes minutes hypoglycemia + No peak action + draw short-acting and + “don’t make a clear day + Cannot be mixed/prepared intermediate together but cloudy” → remember with any other insulin or basal in a separate when drawing up insulin solution injection + provides glucose control  Insulins + usually pts on a sliding for the patient during fasting scale periods or in between meals. Considerations + Storage of insulin: Do not heat/freeze, In-use vials may be left at room temperature up to 4 weeks, Extra insulin should be refrigerated, Avoid exposure to direct sunlight Administration + IV administration (emergency situations eg. DKA, HHS): Regular insulin is the only insulin that can be administered intravenously, and careful monitoring (e.g., of hourly plasma glucose levels) is required + Fastest absorption from abdomen, followed by arm, thigh, and buttock, Rotate injections within one particular site, Do not inject in site to be exercised + Insulin pump: Continuous subcutaneous infusion, Battery-operated device, Connected via plastic tubing to a catheter inserted into subcutaneous tissue in abdominal wall, Potential for tight glucose control + Insulin pen Problems with + Hypoglycemia, Allergic reaction, Lipodystrophy (breakdown of adipose tissue) insulin therapy + Somogyi effect (glucose renews more than the amount of insulin can handle): Rebound effect in which an overdose of insulin causes hypoglycemia, Occurrence of hypoglycemia that can go undetected during sleeping hours, Counterregulatory hormones released + Dawn phenomenon (can be caused by any type of insulin): Characterized by hyperglycemia present on awakening in the morning → Due to release of counterregulatory hormones in predawn hours, Growth hormone/cortisol possible factors GI and ostomy lab Answers from Chrissy for the GI lab review questions 1. Before you do anything, you should always verify correct placement of the NGT (whether the tubes is in place for enteral feedings or gastric decompression). Next, in this  question, you are getting ready to start the enteral feeding so you should ensure that you have performed a complete abd. Assessment, including auscultation of BS to ensure that they’re not absent. If BS absent, you would have to notify the doctor right away 2. A - correct, B - flush the tubing is vague… when would you flush? With what would you flush? How much? 3. Yes, checking gastric residual is assessing for delayed gastric emptying, or how well your patient is tolerating the EN 4. high fowlers is more related to prevention of complications…comfort care…skin care around the nose to prevent breakdown. What else? 5. the blue port otherwise knows as the « pigtail » is the air vent. You never flush or put meds through this ever. It allows for continuous drainage. It should never be clamped or attached to suction 6. think about why before surgery… patients will commonly have an NGT following surgery to speed the return of bowel function or reduce abdominal distension 7. clinical assessments to ensure correct placement also includes complete abdominal assessment, opening mouth and ensuring the GT is not coiled, no signs of respiratory distress…you would also ensure an X-ray is done when the tube is first placed, and you asses outer marking on the tube to ensure it is at the right spot. PH test can be don, although follow institutional protocols 8. Yes; complete assessment including ensuring the pt understands th purpose of suppository or enema, verifying the medical order and making sure there are no contraindications 10. Sims position is used to ensure that the enema flows downward with gravity along the natural curve of the colon and rectum IV lab Test 2 Test 2 Anemia 1. Describe different types of anemias (anemia caused by decreased RBC production, increased RBC destruction, or blood loss). Anemia: - Deficiency in number of erythrocytes (circulating RBCs) - Quantity & quality of Hemoglobin (Hb) → ⅔ of O2 is in Hem - The volume (percentage) of packed RBCs (Hemtocrit, Hct) Characterized by: Morphology: RBC characteristics (microcytic, normocytic, macrocytic, hypochromic, normochromic) OR Etiology: Underlying cause 2. Describe anemias associated with chronic diseases. 3. Described the diagnostic measures for different types of anemias. 4. Describe nursing assessments and therapeutic management for different types of anemias. 2. Differentiate between iron deficiency anemia (IDA) and other types of anemia. 3. State the incidence and causes that contribute to IDA. 4. Describe the signs and symptoms of IDA. 6. Describe the diagnostic measures and the significance of results for IDA. 8. Differentiate between the therapies used to assist the client with IDA and different types of anemias. 9. List the complications that may result from IDA. 10. List the common adaptation problems in clients with IDA and the related nursing care. Insufficient RBC production Excessive/Premature RBC Blood loss destruction Description Aplastic anemia: Megaloblastic anemia: Hemolytic Sickle cell: IDA (Iron deficiency + pancytopenia (↓ in + group of disorders caused by impaired anemia: + a group of anemia): all blood cell types) DNA synthesis + premature inherited, + lack of healthy RBCs & hypocellular bone + easily destroyable macrocytic (large) RBCs destruction or ↑ autosomal in blood d/t insufficient marrow (↓ RBCs, + Vit B12, Folic acid deficiency rate of hemolysis recessive disorders iron platelets, WBCs) than rate of + vaso - occlusion + congenital or Pernicious anemia: Folic acid production (sickling crisis): acquired + common cause of deficiency: rigid, abnormal + suppression of cobalamin deficiency + lack of folic acide shaped RBCs bone marrow aka B12 deficiency for DNA synthesis → block tissue + inhibition of IF no RBC formation & capillaries, vessels (intrinsic factor) maturation → tissue hypoxia secretion in gastric + develops over time → severe pain → mucosa d/t tissue necrosis → antibodies attacking ↑ risk for wound gastric parietal cells infection + Vit B12 helps + abnormal form maturation of RBCs of Hgb → erythrocyte stiffens & lengthens d/t ↓ O2 Association with + chronic inflammation chronic diseases + Autoimmune diseases + infectious diseases + Malignant diseases + Differentiate from IDA: ↑ serum ferritin & ↑ iron stores + Chronic renal disease: ↓ erythropoietin production & might have blood loss from dialysis + management through correction of undelying disorder; erythropoietin therpaies for renal disease or anemia from cancer therapies Diagnostic + ↓ RBC, Hgb, Hct, serum iron, ferritin, folate & vit B12, serum erythropoeitin levels, + pt history: nutritional measures + low or high reticulocytes, LDH assessment + heme-positive stools + diagnostic test: CBC, + bilirubin or transferrin ferritin + liver enzymes (AST, ALT, Albumin, total protein) + liver function test + stool occult blood test + endoscopy (for small gut) & colonoscopy (thru. Anus - polyps, injuries, bleeding) to detect GI bleeding + bone marrow biopsy Nsg assessments + treat cause + follow-up & ensure Teaching + Diet teaching (↑ & therapeutic restoring compliance with + decrease triggers intake of food with iron management pancytopenia therapy (cold weather, - liver & muscle meats, + prevent + protect from stress, ↑ altitudes) eggs, dried fruits, complication from injuries, burns & + ongoing legumes, leafy infection & trauma → ↓ screening (for dark-green veggies, hemorrhage sensations to heat & retinopathy, brain whole-grain & enriched + limit high dose pain d/t neurological scans) bread, cereals, beans, corticosteroids → impairement; + up to date soy) immunosuppression evaluate skin often if immunizations in elderly on heat therapy (prevent complications) Subjective: + Meds: Iron & vit supplements, herbal products, antineoplastic (prevent tumor cells from growing & dividing), antireoviral, anti-coags, NSAIDS, anti-convulsants + PMHx.: recent blood loss, trauma, chronic illness, Hx. of travelling, exposure to infection + Sx./treatments: recent Sx., small gut resection, gastrectomy (removal of a part of the stomach - bypassing duodenum & rapid transit of food → ↓ iron absorption), prosthetic heart valves, chemotherpay & radiation, hemodialysis + Nutrition + GI (N/V, heartburn, painful tongue) + Oxygenation + Elimination + Sexual reproduction Objective: + look for S&S of all systems Causes/risk + chronic alcoholism + inadequate diet factors + GI surgery + malabsorption of iron + IBD (inflammatory (GI sx [sx: signs & bowel disease) → symptoms]) → chronic inflammation duodenum disease interferes with iron + chronic GI blood loss absorption in small + menstruation gut and also d/t slow + blood loss from blood loss dialysis + hemolysis (CKD) + alcoholism S&S + fatigue + Pallor + dyspnea + glossitis + susceptible to + cheilitis infection (inflammation of the + bleeding lips) + headache + paresthesia (feeling of tingling, numbness under skin) + burning sensation of  the tongue + hemoptysis (coffee, bloody vomit): blood in