NURS 2535 Final Exam Review PDF

WEEK 1 -​ Trade = proprietary (trade school → building → property) -​ Drugs classified by structure and therapeutic use -​ Pharmaceutics = influence of drug forms -​ Pharmacodynamics = drug’s effect on the body -​ Pharmacokinetics = body’s effect on the drug -​ Time-critical = with...

WEEK 1 -​ Trade = proprietary (trade school → building → property) -​ Drugs classified by structure and therapeutic use -​ Pharmaceutics = influence of drug forms -​ Pharmacodynamics = drug’s effect on the body -​ Pharmacokinetics = body’s effect on the drug -​ Time-critical = within 30 minutes before or after -​ Non-time critical = within 2 hours before or after WEEK 2 -​ X-rays: -​ With(out) contrast -​ Bones -​ Sinuses -​ Lungs -​ Colon (barium) -​ Planes -​ Computed tomography (CT): -​ Space-occupying lesions (tumors, abscesses, infarcts) -​ Urinary tract -​ Arteries -​ Best for acute and delineating deep-seated lesions -​ Cross-sectional -​ MRI: -​ Bone, joint, brain, spinal cord lesions -​ Planes -​ Displace protons -​ Ultrasound: -​ Gallbladder -​ Uterus -​ Echocardiogram -​ Best between soft tissue and liquid -​ Nuclear isotope scans (PET): -​ Altered tissue uptake of substance -​ Biopsy is small -​ Resection is large WEEK 3 -​ Drugs bind to albumin therefore can’t distribute -​ K in ICF -​ Na in ECF -​ Stress, nausea, nicotine, and morphine stimulate ADH  -​ Aldosterone ↑ Na and K -​ Fluid and electrolyte imbalances caused by burns or heart failure -​ ECF volume deficit = hypovolemia: -​ Diarrhea -​ Fistula drainage -​ Hemorrhage -​ Plasma-to-ISF shift -​ Treat with IV solutions -​ Fluid volume excess = hypervolemia: -​ Abnormal fluid retention -​ Interstitial-to-plasma fluid shift -​ Treat by changing electrolyte composition or ECF osmolality Hyper Hypo Natremia: (hyperactive nature has ticks) Natremia: Thirst CNS deterioration Increased ISF Nausea CNS deterioration Vomiting Kalemia: (lots of kale triggers Vecna) Kalemia: (Beck eats a little bit of kale) Ventricular fibrillation Bradycardia ECG changes ECG changes CNS changes CNS changes (Tx: IV insulin, diuretics, Na bicarbonate, IV Ca gluconate) Calcemia: (same as hypernatremia) Calcemia: Thirst Laryngeal stridor Increased ISF ECG changes CNS deterioration Tetany (Tx: diuretics, calcitonin, isotonic saline, CNS changes mobilization) Chvostek’s sign Tingling Dysphagia -​ Na role: -​ ECF volume and concentration -​ Nerve impulse generation and transmission -​ Acid-base balance -​ K role: -​ Nerve and muscle impulse conduction and transmission -​ Cellular growth -​ Cardiac rhythm maintenance -​ Acid-base balance -​ Ca role: -​ Nerve impulse transmission  -​ Myocardial contractions -​ Blood clotting -​ Muscle contraction -​ Hypotonic (maintenance) IV fluid causes water to move from ECF to ICF -​ Isotonic IV fluid causes ECF expansion (lactated ringer’s, D5W, normal saline) -​ Hypertonic IV fluid causes ECF expansion and increased osmolality (monitor BP, lung sounds) (D5 ½ normal saline) -​ Normal pH = 7.35 to 7.45 -​ Bones, lungs, kidneys regulate acid-base balance -​ Buffers bind to excess H+ or OH- without large pH change -​ Carbonic acid-bicarbonate is plasma-buffer system -​ ↑ respiration = ↑ H+ -​ pH 7.4 = bicarbonate to carbonic acid ratio of 20:1 -​ Respiratory = CO2 -​ Renal = H+ and HCO3- -​ Protein = hemoglobin buffer for H+ -​ Metabolic acidosis = ↓ HCO3- WEEK 4 -​ Pharmacogenetics = genetic variations in drug response, single-gene variations -​ Pharmacogenomics = individualized drug therapy based on a patient’s genetic makeup -​ Drugs commonly involved in severe medication errors: CNS drugs, anticoagulants, chemotherapeutic drugs WEEK 5 -​ Thrombus = blood -​ Embolus = particulate -​ Apoptosis: -​ “Programmed cell death” -​ No inflammation -​ No elicit inflammatory response -​ Not necessarily indication of injury -​ Neutrophils and macrophages do phagocytosis -​ Pain is prostaglandins and histamine -​ Bradykinin activates nociceptors (pain) -​ Macrophage release IL-1 and TNF -​ Phagocytes primarily move to injury site -​ Histamine dilates -​ Fibrinogen causes coagulation -​ C5a causes chemotaxis and permeability -​ C3a causes permeability -​ IL-10 and TGF down-regulate and resolves acute inflammation -​ Chronic inflammation predominantly lymphocytes, plasma, and macrophages -​ Transudate = water, low protein  -​ Exudate = obstructed lymphatic flow -​ Serous exudate = some protein, lesser damage -​ Purulent exudate = live and dead leukocytes WEEK 7 🩸👶∞ -​ B and T cells first release cytokines 💧 G 🥇 A 😷 M E DⒷ -​ Elderly increased apoptosis of B and T cells -​ Type 1 hypersensitivity reaction is IgE mediated (T-helpers → B cells → IgE → mast cells and basophils -​ Type 2 hypersensitivity reaction caused by IgG and IgM antibodies that bind to antigen → macrophages -​ Type 3 hypersensitivity reaction = circulating antigen-antibody complexes trigger complement system -​ Type 4 hypersensitivity reaction = delayed, T cells, cytokines Type 1 Type 2 Type 3 Type 4 -​ ↑ eosinophils, -​ ↓ blood cells -​ Examples: -​ ↑ lymphocytes IgE, atopic -​ Examples: -​ Glomerul and allergens -​ Erythrobl onephritis macrophages -​ Examples: astosis -​ Polyarteri -​ Examples: -​ Asthma fetalis tis -​ Poison -​ Allergic -​ Blood nodosa ivy rhinitis transfusio -​ Contact -​ Urticaria n dermatitis -​ Angioede reaction ma -​ Autoimm -​ Anaphyla une xis hemolytic -​ GI food anemia allergies and thromboc ytopenia -​ T cells made in marrow, mature in thymus -​ Monocytes → Macrophages -​ Lymphocyte → natural killers -​ Hematopoietic drugs use recombinant DNA technology to decrease chemo-induced anemia, neutropenia, and thrombocytopenia so higher chemo dose can be given -​ Hematopoietic drugs cause fever, muscle and bone pain, flushing -​ Erythropoietic drugs: -​ Epoetin and darbepoetin alfa = produces erythropoietin hormone to make RBCs for those with renal failure -​ Colony-stimulating factors: -​ Filgrastim and pegfilgrastim = ↑ WBCs (granulocytes like baso,eosino, neutrophils) caused by chemo drugs -​ Interferons: -​ Protein -​ Antiviral, antitumour (Stop division and replication), immunomodulating (increase other WBC and NK cells) -​ Treat cancer, viruses (warts, hepatitis), MS -​ Alpha, beta, and upsilon (Y) -​ Similar to IFN cytokines -​ Cause flu-like symptoms -​ Monoclonal antibodies: -​ Treat cancer, RA, MS, and organ transplant rejection -​ Don’t affect healthy cells as much -​ Interleukins: -​ Lymphokines (natural) -​ Antitumour (IL-2 activated by T cells) -​ Agonists (IL-6, aldesleukin, anakinra) -​ Aldesleukin binds to T cell sites to multiply and renal and skin cancer, NOT FOR ORGAN TRANSPLANT, ONLY INJECTION -​ Aldesleukin toxicity can cause capillary leak syndrome/fluid retention, reversible -​ Anakinra is IL-1 receptor antagonist, controls RA -​ Anti organ rejection drugs: -​ Glucocorticoids stop all T cell activation -​ Calcineurin inhibitors stop phosphate use for IL-2 production -​ Antimetabolites stop cell proliferation -​ Biologics stop cytotoxic T killer cell function -​ Cyclosporine (narrow therapeutic range) -​ Common infectious organisms: -​ H. pylori → gastric lymphoma and adenocarcinoma -​ Non specific symptoms (fever, rapid pulse, muscle aches, malaise, inflammation at site) -​ Neutrophils: bacteria -​ Lymphocytes: viruses -​ Staph: -​ G(+) -​ Pus -​ Flora of respiratory tract and skin -​ Skin and deep soft-tissue abscesses  -​ S. pneumoniae causes pneumonia, otitis media, meningitis -​ V. streptococci in mouth, cavities -​ Group A strep causes impetigo, cellulitis, necrotizing fasciitis -​ G(-) rods: -​ E.coli -​ Klebsiella -​ Enterobacter -​ Fungal infection is opportunistic in hyphal phase, causes acute inflammatory response -​ Fungi into blood cause angioinvasion, IV treatment Common allergies Sulfonamides -​ Stop metabolism -​ Combination therapy -​ Bacteriostatic -​ Stop folic acid synthesis -​ G(+) and G(-) -​ UTIs, upper respiratory tract infections (staph) Penicillins (B-lactam) -​ Enter via cell wall -​ Stops cell wall synthesis -​ G(+) -​ NO NSAIDs, oral birth control, Warfarin -​ Bactericidal Cephalosporins (B-lactam) -​ Semisynthetic -​ Similar to penicillins -​ Bactericidal -​ Progressively gets better at treating G(-)  -​ UTIs Macrolides -​ Stop protein synthesis -​ “-cin” -​ Bacteriostatic -​ High concentration is bactericidal -​ Strep Carbapenems -​ Broadest -​ Complicated body cavity and connective tissue infections -​ Infused over 60 minutes -​ Seizures Monobactams (B-lactam) -​ Synthetic -​ G(-) aerobes -​ Bactericidal -​ PARENTERAL ONLY -​ Cystic fibrosis Tetracyclines -​ Stop protein synthesis -​ Semisynthetic and natural -​ Bacteriostatic -​ AVOID DAIRY, ANTACIDS, IRON SALTS -​ AVOID IF < 8 OR PREGNANT/LACTATING -​ Tooth discolouration -​ G(+) and G(-) Aminoglycosides -​ Natural and semisynthetic -​ NOT ORAL -​ Serious toxicities -​ Bactericidal -​ Stop protein synthesis -​ G(-) and G(+) -​ Combination Fluoroquinolones -​ AVOID DAIRY, ANTACIDS, IRON, MAGNESIUM -​ G(-) and G(+) -​ Bactericidal -​ Alters DNA WEEK 11 -​ Invasion is to close by area -​ Metastasis is to entirely new site -​ Cancer grows on top of or between normal cells -​ Differentiation: -​ Orderly process -​ Immaturity to maturity  -​ Stable -​ Will NOT dedifferentiate -​ Not completely understood -​ Endoderm = trachea, lungs, epithelium -​ Mesoderm = muscles, bones, CT -​ Ectoderm = brain, skin, glands -​ Proto-oncogenes and tumour suppressor genes can be affected by mutation Benign Malignant -​ Well-differentiated -​ Undifferentiated -​ Encapsulated -​ Infiltrative and expansive growth -​ Expansive growth -​ Recur -​ Rarely recur -​ Moderate to marked vascularity -​ Rarely encapsulated -​ Less like parent cell -​ Rapid growth -​ Large nucleoli -​ Carcinoma = epithelial tissue (carcass → skin) -​ Sarcoma = mesenchymal or CT (sarcophagus → ancient → museum) -​ Leiomyoma = smooth muscle (lei → Hawaii → Hawaiian people are strong → muscle) -​ Chondroma = cartilage -​ Adenoma = glandular or columnar epithelium (a den → house → made of columns) -​ Very few mutations lead to cancer -​ Single alteration does NOT cause cancer -​ Neoplasms: -​ Behave like parasites -​ Respond to growth promoting stimuli -​ Only one allele needs to mutate for altered protein function and phenotype effect -​ APC = signal transduction inhibition = colon cancer -​ P16/INK4 = cell cycle regulation = melanoma (ink → dark → melanin → melanoma) -​ Aflatoxin = liver cancer -​ Azo dyes = bladder cancer -​ Benzene = leukemia -​ Vinyl chloride = angiosarcoma -​ Coal tar = scrotal cancer -​ Mono = burkitt lymphoma -​ Dysplasia = neoplastic clone, atypical appearance, localized, not always malignant, low grade to high grade, carcinoma precursor -​ Malignant cells destroy basement membrane and move into blood supply -​ TNM: -​ T = tumor description -​ N = lymph node metastasis extent -​ M = distant metastasis has occurred -​ Stage 1 = local manifestation -​ Stage 4 = metastatic spread -​ Malignant neoplasms can be detected by imaging modalities -​ Lung, breast, and prostate cancers metastasize to bone -​ Immunohistochemistry = estrogen receptor -​ Microarray technology = gene chips -​ Cancer death = infection, cachexia, metabolic/endocrine effects, hemorrhage -​ Chemo: -​ Narrow TI -​ Combo -​ Harmful to all rapidly growing cells (follicles, GI, bone marrow) -​ Imatinib (the mat nipped off the enzyme): -​ Miscellaneous -​ Antineoplastic -​ Treats chronic myeloid leukemia  -​ Targeted therapy NOT a monoclonal antibody -​ Inhibits enzyme -​ Interact with hepatic-metabolized drugs -​ Many adverse effects and interaction -​ Mitotane: -​ Miscellaneous -​ Antiadrenal -​ Ask about GI symptoms -​ Hydroxyurea: -​ Miscellaneous -​ Antineoplastic -​ Antimetabolite (interacts with DNA synthesis) -​ Treats squamous cell carcinoma and leukemias -​ Many adverse effects -​ Bevacizumab (the bee vacuum blocks the blood): -​ Miscellaneous -​ Angiogenesis inhibitor -​ Blocks blood supply to growing tumour -​ Treats metastatic colon cancer, rectal cancer, non-small cell lung cancer, malignant glioblastoma -​ Many adverse effects (nephrotoxicity) -​ Extravasation: -​ Leaking of IV antineoplastic onto surrounding tissue -​ Destroy nerves, tendons, muscles -​ Grafting and amputation -​ If occurs, STOP infusion and contact prescriber LEAVE IV CATHETER IN PLACE, aspirate residual drug/blood from catheter, hot/cold over site, sterile occlusive dressings, elevation WEEK 12 -​ Respiratory distress: -​ ↑ work of breathing and rate even if normal oxygenation ability -​ Respiratory failure: -​ Inability to fulfill gas exchange -​ Abnormal O2 and CO2 -​ O2 < 60 -​ CO2 > 50 -​ Hypoxia: -​ Results in anaerobic metabolism (lactic acid produced) → metabolic acidosis -​ Mild: -​ Tachycardia (heart beats more to try and deliver oxygen) -​ Peripheral vasoconstriction (conserve oxygen) -​ Diaphoresis (sweating) -​ Mild BP increase  -​ Moderate-severe: -​ CNS changes -​ Cyanosis -​ Bradycardia -​ Hypotension -​ Hypercapnia: -​ Inversely related to alveolar ventilation -​ Respiratory acidosis -​ Abnormal kidney, nervous, and cardiovascular function -​ Treat with respiratory muscle training, CPAP, mechanical ventilation -​ Asthma: -​ Leading cause of child hospitalization in Canada -​ One Canadian/day dies from asthma -​ Triggers cause mast cell degranulation,IL-4, and IgE production -​ Primary response = chronic inflammation → airway hyperresponsiveness -​ Causes prolonged expiration -​ Treat with inhaled corticosteroid, leukotriene modifiers, monoclonal IgE antibody -​ Bronchodilators (B2-adrenergic agonists, methylxanthines, anticholinergics) -​ Severity measured with flow rates -​ Severe asthma treated with IV corticosteroids, IV Mg sulfate, O2, IV fluids -​ COPD: -​ Chronic bronchitis and emphysema -​ Abnormal inflammatory response of lungs to noxious particles/gases -​ Women die more than men -​ Forced exhalation from loss of elastic recoil and obstructed airflow from mucus, edema, and bronchospasm -​ Barrel-chest, weight loss, cough, thick/odorous/discoloured sputum, dyspnea on exertion, tripod stance, pursed lips, expiratory wheeze/crackles, hypoxia, hypercapnia, cyanosis, polycythemia (excess RBC) -​ Diagnose with pulmonary function test (low O2, high CO2, low pH, high bicarbonate in late stages) -​ Smoking cessation most effective -​ Bronchodilators (B2-adrenergic agonists, methylxanthines, anticholinergics) decrease dyspnea and increase forced expiratory volume -​ Thickened blood vessels -​ Pulmonary hypertension → RV hypertrophy → heart failure (R-side) -​ Chronic bronchitis: -​ Inflamed bronchial lining -​ Excess mucus -​ Emphysema: -​ Enlarged alveoli -​ Collapsed bronchiole -​ Smoking and inherited alpha1-antitrypsin deficiency cause macrophages and neutrophils to release elastase to decrease alpha1-antitrypsin and destroy elastic fibers -​ Pneumonia: -​ Acute inflammation of lung parenchyma → aspiration (usually ↓ LOC) -​ Bacteria, virus, fungi, parasites, chemical cause -​ Opportunistic -​ Alveoli thickening and fluid accumulation Community acquired Hospital acquired -​ S. pneumoniae -​ P. aureus -​ Mycoplasma -​ Enterobacter -​ Viruses -​ E. coli -​ C. pneumoniae -​ Klebsiella -​ MRSA -​ S&S: -​ Sudden onset fever -​ Chills -​ Productive (mucus) cough -​ Purulent (yellow) sputum -​ Dyspnea -​ Tachypnea -​ Toxic look -​ Pleuritic chest pain -​ Dull percussion -​ ↑ fremitus -​ Bronchial breath sounds -​ Crackles -​ Treatment: -​ O2 -​ Analgesics -​ Antipyretics -​ Antibiotics -​ Rest -​ Oral/IV hydration -​ Respiratory distress syndrome: -​ Alveoli surfactant lowers surface tension to prevent atelectasis (lung collapse) -​ Insufficient surfactant causes alveoli collapse and resistance to opening -​ Inflammatory exudate and proteinaceous precipitate in dilated bronchioles and alveolar ducts stops gas exchange -​ O2 helps but causes additional injury to alveolar lining -​ Treatment: -​ Glucocorticoids to mother before delivery to increase surfactant -​ Exogenous surfactants -​ Intratracheal surfactant through endotracheal tube within 30-60 min of birth -​ Pulmonary hypertension stops blood from going into lungs  -​ S&S: -​ Tachypnea -​ Expiratory grunting -​ Nasal flaring and retractions -​ Cyanosis -​ Cystic fibrosis: -​ Exocrine gland dysfunction -​ Most common lethal genetic illness among caucasian kids -​ Autosomal recessive -​ Increased mucus viscosity -​ Increased sweat electrolytes (Na, Cl) -​ Increased organic and enzymatic saliva components (Na, Cl) -​ ANS abnormalities -​ Affects bronchi, small intestine, pancreatic ducts, bile ducts (obstruction and hypertension in bile ducts) -​ Bronchial epithelium destroyed -​ Infection spreads to peribronchial tissue and weakens bronchial walls -​ S&S: -​ Atelectasis -​ Hyperinflation -​ Stagnant mucus (destroy lungs and favour bacterial growth) -​ Peribronchial fibrosis -​ Decreased O2 and CO2 exchange → contraction and hypertrophy of muscle fibers in pulmonary arteries and arterioles -​ Pulmonary hypertension -​ Cor pulmonale (R-sided heart failure) -​ Pneumothorax -​ Hemoptysis -​ Nasal polyps -​ Treatment (no cure): -​ Chest physiotherapy -​ Bronchodilator -​ Forced expiration -​ Aggressive home IV/aerosolized antibiotics -​ NSAIDs -​ Transplantation (liver, heart, lung, and pancreas) -​ Nutrition -​ Chest drainage:​ -​ Tube into pleural space to drain fluid/air (28 to 32 size for adults -​ Tube inserted higher (2-3 intercostal) if air, lower (4-6 intercostal) if fluid -​ Allows normal intra-pleural/pulmonic (negative) pressure -​ Normally pleural space between parietal and visceral pleura is collapsed -​ 3 collection chambers -​ Occlusive dressing, petroleum if needed -​ Tape tube to chest  -​ Check tube patency Q 2-4 hr -​ Drainage >100 ml/hr NOTIFY HCP -​ Tube pain is normal -​ Pleural effusion fluid is straw coloured -​ DON’T MILK TUBING -​ STOP:​ -​ Site -​ Tape -​ Output -​ Patency -​ Report to MD if: -​ Tachypnea -​ Decreased or absent breath sounds -​ Hypoxemia -​ Tracheal deviation -​ Subcutaneous emphysema -​ Neck vein distension -​ Tachycardia -​ Fever -​ Dysrhythmias -​ Tuberculosis: -​ CAN’T be eradicated -​ M. tuberculosis is inhaled -​ M. bovis from infected cow milk -​ Initially asymptomatic -​ Survive phagocytosis and replicate inside macrophages -​ Macrophages form granulomas -​ Secondary TB causes tissue necrosis, destroying lung tissue and bronchial walls -​ Tubercle bacilli: -​ Multiply unchecked within areas of necrosis -​ Present in large numbers in sputum and expectorated necrotic debris -​ May disseminate to other organs -​ Screening for TB -​ Irregular, spiculated lesion = TB -​ Pleural effusion -​ Dull/low-pitched lung sounds