Inflammatory (Nonselective COX Inhibitors) Acetic Acid: Diclofenac Etodolac Indomethacin Sulinclac Tolmetin Propinonic Acid: Fenoprofen Flurbiprofen

Ibuprofen Ketoprofen Naproxen Oxaprozin Fenamate: Meclofenamate Meclofenamic acid Salicylate: Aspirin Diflunisal Naphthylalkanone: Nabumetone Oxicam: Piroxicam Meloxicam Choline magnesium trisalicylate: Salsalate (Selective COX-2 Inhibitors) Celecoxib Rofecoxib COX-3: Acetaminophen Immunosuppressants (Corticosteroids) Calcineurin Inhibitors: Cyclosporine (Sandimmune) Tracolimus (Prograft) Sirolimus (Rapamune) Cytotoxic Agents: Azathioprine (Imuran) Cyclophosphamide (Cytoxan, Neosar)

Mycophenolate mofetil (CellCept, Myfortic) Leflunomide (Arvara) Methotrexate (Rhumatrex, Trexall) Bioactive Immunosuppressants Anti-thymocyte antibodies: OKT3 (Muromonab-CD3) Antilymphocyte Globulin Antithymocyte Globulin-Rabbit IL-2 Receptor Antibodies: Basilixmab (Simulect) Daclizumab (Zenapax) Antihistamines: First Generation: Dipenhydramine Promethazine Brompheniramine Diphenhydramine Chlorpheniramine Dexchlorpheniramine Cyproheptadine Hydroxyzine Clemastine Promethazine Tripolidine Second Generation: Azlastine Cetirizine Desloratidine Loratadine Fexofenadine Type 1 Hypersensitivity: Epinephrine Dopamine/Dobutamine Type 2 Hypersensitivity: Blood & Saline Dipenhydramine Type 3 Hypersensitivity: Aspirin or NSAID Plaqeunil Steroids Immunosuppressants: Azathioprine (Imuran) Cyclophosphamide (Cytoxan)

Cyclophosphamide (Sandimmune) Mycophenolate (CellCept) HIV: PCP: Trimethoprim Sulfamethoxazle-Cotrimoxazole (Bactrim) TB: Drug interaction between Protease Inhibitors & Rifampin 4 Types of Anti-virals: 1. Reverse Transcriptase Inhibitors (NRT & NNRT) a. Zidovudin AZT (Retrovir, Zidobudin) b. Didanosine (DDI) (Videx) c. Zalcitabine (DDC) (Hivid) 2. Protease Inhibitors a. Saquinavir b. Ritonavir c. Intinavir 3. Entry/Fusion Inhibitors a. Enfuvirtide (Fuzeon) 4. Nucleoside reverse transcriptase inhibitors a. Zidovudin AZT (Retrovir) HAART Others: Stavudin (Zerit) Lamividine (Epivar) Zidovudin (AZT, Retrovir) Marinol Megace Fe Deficiency Anemia Oral Iron Salts: Ferrous sulfate, ferrous lactate, ferrous fumarate IV Iron Dextran B12 Deficiency Anemia Vitamin B12 (Cobalamin) Injection Folic Acid Deficiency Anemia Vitamin B9 Supplement

Aplastic Anemia Blood transfusion Bone Marrow transplant Immunosuppressive therapy Sickle Cell Anemia Folic Acid Supplements Blood transfusion Genetic counseling Hematopoietic Stimulants: Epoetin Alfa (Procrit & Epogen) Darbepoetin Alfa (Aranesp) Neutropenia & Immunostimulants: Colony Stimulating Factors: Granulocyte colony stimulating factor (G-CSF) Filgastim (Neupogen) Pegfilgastim (Neulasta) Granulocyte macrophage stimulating factor (GM-CSF) Sagramostim (Leukine) Thrombocytopenia: ITP: Steroids & Immunosuppressants Plasmapharesis Transfusion of platelets Splenectomy TTP: Plasmapharesis Cryosupernatant plasma & Solvent deterent plasma DO NOT TRANSFUSE PLATELETS HIT: NO HEPARIN OR HEPARIN PRODUCTS Argatroban Lepirudin Fondaparinux (Arixtra) Cancer: Cell-Cycle Nonspecific: Alkylating Agents Nitrogen Mustard (Mechlorethamine HCl) Cisplatin Cyclophosphamide

Nitrosureas (Carmustine, Lamustine, Semustine) Anti-tumor Antibiotics Actinomycin D Bleomycin Adriamycin (Doxorubicin) Cisplatin Nitrosureas Cell-Cycle Specific: Antimetabolites Methotrexate 5 Fluorouracil 6 Mercaptopurine *Leucovorin Rescue Mitotic Inhibitors Vincristine Vinblastine Bleomycin Antibiotics Vinca alkaloids Etoposide Hormones: Tamoxifen (Novaldex) Flutamide Nilutamide Bicalutamide Immunotherapy: Monoclonal Antibodies Trastuzmab Rituximab Bevaxizmab Cetuximab BCG (Bacillus-Calmette & Guerin)

Drugs to Know: 1. Inflammatory Process - NSAIDS - COX 2 Inhibitors - Leukotrien Inhibitors COX 1 PG12: Gastric mucosal integrity Gastric Irritation- instruct to take with meal and full glass of water PGE2: Bronchodilation, renal function by dilating renal arterioles trigger asthma attack, decrease GFR and Na Retention Contraindicated with CHF and Renal insufficiency (BUN & Creatinine elevated) TXA2: Platelet function risk for bleeding monitor for bleeding & assess if patient is taking anticoagulants - *More side effects! COX 2 PGE2 & PGF2a: Inflammation anti-inflammatory effect- monitor for efficacy, therapeutic Nonselective COX Inhibitors Acetic Acid Propionic Acid Diclofenac Etodolac Indomethacin Sulinclac Tolmetin Fenoprofen Flurbiprofen Ibuprofen Ketoprofen Naproxen Oxaprozin Fenamate Salicylate Naphthylalkanone Oxicam Nabumetone Piroxicam Meloxicam Choline magnesium trisalicylate Salsalate

Meclofenamate Aspirin Meclofenamic Diflunisal acid

Selective COX-2 Inhibitors Celecoxib Rofecoxib *Lesser side effects Dont take if at risk for blood clots! Risks for clotting-HA, stroke, etc. Aspirin - Salicylate NSAID o Antipyretic o Analgesic o Anti-inflammatory o Prophylaxis of diseases due to platelet aggregation - Thromboxane A2 stimulates blood platelet aggregation, essential to the role of platelets in blood clotting. - *The effect of aspirin is long lived because platelets lack a nucleus and do not make new enzyme - At risk for bleeding - 81 mg everyday = anti-platelet - Surgery: hold 7-10 days; Emergency: platelet transfusion Side Effects: same as other Non-Selective COX inhibitors Toxic Effects: Ototoxic, Hepatotoxic, Nephrotoxic, Reyes Syndrome: high fever, vomiting, liver dysfunction, unresponsiveness, delirium, convulsions, coma, possible death, common in children. Acid-Base Imbalance: fluids, bicarbonate, electrolytes, hemodialysis

COX Cox 1 Cox 2 Cox 3

Function Organ pain, platelet function, stomach protection Inducible: inflammation, pain, fever

Inhibitor NSAIDs including aspirin NSAIDs, COX 2 inhibitors including celebrex Acetaminophen & some NSAIDs

Pain pathways, not inflammation pathways Tylenol: only pain not inflammation. Max 24 hours is 4 grams

Pregnancy & NSAIDs: Category C- drugs that have not been studied in pregnant humans but that do appear to cause harm to the fetus in animal studies. May still be given to a pregnant woman if her healthcare provider believes that the benefits outweigh the risks to her unborn childAvoid taking NSAIDs at all during the 3rd trimester. Prolongation of gestation and inhibitor of labor. Risk for Patent Ductus Arteriousus 2. Immunosuppressants Corticosteroid Adverse Effects: - All commonly occur because high doses used for immunosuppression: o Cushings Syndrome Hyperglycemia (Gluconeogenesis) Weight gain (Na & H2O retention) Abnormal fats distribution Hypertension Hypokalemia o Gastric Ulcer o Euphoric personality changes o Osteoporosis Inhibition of osteoblastic activity, decreased calcium absorption, increased urinary calcium excretion o Cataracts Calcineurin Inhibitors : interleukin 2 production blockers Cyclosporine (Sandimmune) Tracolimus (Prograft) Adverse Effects: Adverse Effects: - Nephrotoxicity - Nephrotoxicity - Hepatotoxicity - Increased risk of lymphoma - Hypersensitivity - Hirsutism - Neurotoxicity - GI complaints - Hypertention - Lymphoma - Anaphylaxis Drug Interactions: Drug Interactions: - Induction and inhibition of - Agents that inhibit CYP3A (an hepatic cytochrom: P450 isozyme of cytochrome P450) - Nephrotoxic drugs - Grapefruit juice - Grapefruit juice (inhibits - NSAIDs p450)

Sirolimus (Rapamune) Adverse Effects: - Raises levels of cholesterol and triglycerides - Thrombocytopenia - Severe complications in the liver and lung - Nephrotoxic (increases incidence when combined with cyclosporine) Drug Interactions: - Hepatic metabolism by CYP450A4 - High fat foods, Grapefruit Juice

Cytotoxic Agents T-Cells & B-Cells Proliferation Blockers 1) Azathioprine (Imuran) 2) Cyclophosphamide (Cytoxan, Neosar) 3) Mycophenolate mofetil (CellCept, Myfortic) 4) Leflunomide (Arvara) 5) Methotrexate (Rhumatrex, Trexall) Adverse Effects: - Bone Marrow Suppression-Pancytopenia - GI disturbance (ANV) - Hepatotoxicity - Nephrotoxicity - Respiratory Function - Increase risk for secondary neoplasia - Cyclophosphamide Hemorrhagic Cystitis Bioactive Immunosuppressants Anti-thymocyte antibodies 1) OKT3 (Muromonab-CD3) a. Monoclonal antibody to CD3 on T cell i. Actions & Uses 1. Blocks all T cell function 2. Inhibits cytotoxic T killer cell function 3. Opsonizes circulating T lymphocytes and enhances their removal a. Depletes T cells prior to bone marrow transplant b. Used to prevent or reverse acute graft rejection 4. Problem with Muromunab antibody is the formation of anti-OKT3 antibodies which limit its action a. Only given by IV infusion for 7-14 days 2) Antilymphocyte Globulin 3) Antithymocyte Globulin-Rabbit - Used to treat acute rejection transplant - Mechanisms o Removal of T cells from circulation o Decrease cytokine induced reactions - Adverse Effects o Hypersensitivity reactions may occur with nonhuman antibodies resulting in: Chills Fever Thrombocytopenia Erythema Pruritis

IL-2 Receptor Antibodies Basilixmab (Simulect) & Daclizumab (Zenapax) - Monoclonal antibody against human IL-2 receptor alpha subunit of activated T cell - Blocks activation and inhibits clonal expansion of T cells - Used to induce immunosuppression and to prolong organ transplants in combination with other immunosuppressants Nursing Implications - Thorough assessment should be performed before administering these agents. o Renal, liver, cardiovascular & respiratory function o Baseline CBC o Clients need to be told that lifelong therapy with immunosuppressants is indicated with organ transplantation & some autoimmune disorders Priority Nursing Diagnosis - Risk for infection o Hand washing o Mask o Use of strict aseptic technique in caring for IV lines, urinary catheter & wound care o Assess frequently for infection Observe the oral cavity often for white patches on the tongue, mucous membranes, and oral pharynx Monitor VS with O2 sat every 4 hours Report fever, tachypnea, tachycardia, hypotension, restlessness, change in O2 saturation o Neutropenic Precaution: Reverse isolation-positive pressure (air out) No fresh flowers or raw foods (peppers) Limiting visitors esp. with infection, colds or flu o Clients taking immunosuppressants should be encouraged to take measures to reduce the risk of infection Avoiding crowds Avoiding people with colds or other infection o Clients should be told to report any fever, sore throat, chills, joint pain, fatigue, or other signs of a severe infection immediately Cytotoxic Agents o Azathioprine (Imuran), Cyclophosphamide (Cytoxan), Cyclosporine (Sandimmune), Mycophenolate mofetil (CellCept) Bone Marrow Suppression Risk for infection Anemia o Blood transfusion o Administer Procrit as ordered o Supplemental oxygen Platelet <75,000

o o o

Bleeding precaution Monitor for abnormal bleeding Avoid ASA &NSAIDs

3. Antihistamines: - Histamine (H1) receptor antagonists bind to H1 receptors - This prevents histamine from binding to its receptor and causing allergic response - Indications o Allergic Rhinitis o Prevention of anaphylaxis o Allergic conjunctivitis o Drug Allergies o Allergic dermatologic conditions o Blood Transfusion First Generation Second Generation Bind to both central and peripheral H1 receptors Bind to peripheral H1 receptor Causes drowsiness Does not cross BBB Possess anticholinergic effects Non-sedating Some are used for motion sickness (30-60 min) - Dipenhydramine - Promethazine Brompheniramine Azlastine Diphenhydramine Cetirizine Chlorpheniramine Desloratidine Dexchlorpheniramine Loratadine Cyproheptadine Fexofenadine Hydroxyzine Clemastine Promethazine Tripolidine Patient Teaching - Contraindicated in pregnancy - 1st generation contraindicated in Glaucoma, peptic ulcer disease, and urinary retention-makes it worse - Do not perform activities that requires attention as antihistamines may cause alcohol - Do not take 1st generation antihistamines during acute asthma, bronchitis, or pneumonia - Do not take more than one antihistamine at a time - Report adverse reactions from the body - Give with food except Loratadine. Cetrizine and Desloratadine may be given with or without food - Monoamine oxidase inhibitors (MAOI) increases duration of action of antihistamines as well as side effects. - Efficacy of Fexofenadine decreases when given with Riampin - Cimetidine, Azole antifungal, & Macrolides increases the effects of loratidine 4. Type 1 Hypersensitivity: Epinephrine: - Place in modified Trendelenburg, start IV with normal saline or LR - Medication of choice for anaphylaxis - SC or IM; 0.01 mg/kg may repeat every 20-30 min prn

Monitor for cardiac arrhythmias! Rapid onset of action, reverses action of Histamine and decreases release from mast cells. o Dilates Bronchioles o Constricts Blood Vessels o Decreases capillary permeability o Stimulates the reformation of tight junction between endothelial cells Side Effects: o Increased pulse rate, pallor, dizziness, chest pain, headache, nausea, vomiting, excitability, anxiety (decreased parasympathetic) neurotransmitter for sympathetic.

Dopamine/Dobutamine: increases blood pressure To further reduce symptoms after lifesaving measures, control: - Antihistamines - Corticosteroids such as Prednisone - Cromolyn Sodium (Intal)-Mast cell stabilizer - Benadryl, Epipen 5. Type 2 Hypersensitivity: - Blood & Saline - Pre-medicate transfusions with Dipenhydramine 6. Type 3 Hypersensitivity: - Mild SLE may be managed with aspirin or other NSAID o Aspirin: prevent thrombosis o Plaqeunil: For skin and arthritic manifestations Reduce frequency of acute episodes - For clients with life threatening symptoms high doses of corticosteroids are given to prevent major organ damage. o Steroids: tapered down as symptoms subside Side Effects: Risk for infection, Mood Swings, Cushings Syndrome, Ulcerogenic, Osteoporosis, Cataracts o Immunosuppresants: may be used alone or in combination with corticosteroids Azathioprine (Imuran) Cyclophosphamide (Cytoxan) Cyclophosphamide (Sandimmune) Mycophenolate (CellCept) Side Effects o Bone Marrow suppression Anemia Administer Procrit as ordered Risk for infection Risk for bleeding *Avoid aspirin & NSAIDs

7. HIV: Opportunistic Infections - PCP o When CD4 count <200, prophylactic RX is started Trimethoprim, sulfamethoxazle-Cotrimoxazole (Bactrim) - TB o Drug interaction between Protease Inhibitors & Rifampin 4 Types of Anti-virals: 1) Reverse Transcriptase Inhibitors (NRT & NNRT): a. Competitive Enzyme Inhibitors i. Zidovudin AZT (Retrovir, Zidobudin) ii. Didanosine (DDI) (Videx) iii. Zalcitabine (DDC) (Hivid) 2) Protease Inhibitors a. Inhibit the viral proteases thus preventing viral maturation i. Saquinavir ii. Ritonavir iii. Intinavir 3) Entry/Fusion Inhibitors a. Interfere with HIV CD4 receptor site binding and entry into cells i. Enfuvirtide (Fuzeon) 4) Nucleoside reverse transcriptase inhibitors- 1st drug a. Zidovudin AZT (Retrovir) first drug approved for HIV b. Aslo used prophylactically for exposures c. Must be taken q4-6 hours round the clock to keep increased blood i. Adverse Effects 1. Bone Marrow toxicity; drug resistance with long term use 2. Nausea and HA most common SE 3. Take hour before or 1 hour after meals HAART Highly Active Anti-retrovial Therapy - Combine 3-4 antiviral drugs o Decreases chance of drug resistance o Does NOT cure disease, can still transmit o Many SE often want to stop meds o Complicated schedules MUST take many time throughout the day MUST adhere to regimen or viral resistance possible or fatality o Expensive! - If prophylactic for occupational exposure or high risk sexual exposure o 4 week course of treatment started within 72 hours of exposure, preferable 2-3 hour

Others: - Used when clients intolerant to AZT o Stavudin (Zerit) - Used with low CD4 cell counts, 1st line treatment in combo with AZT o Lamividine (Epivar) - Used prophylactically after parenteral exposure to HIV? o Zidovudin (AZT, Retrovir) - How is the effectiveness of treatment determined? o Monitoring viral load and CD4 cell counts - When treatment is working the CD4 cell count sould be? o Above 350 mm3 - Appetite Stimulants: o Marinol o Megace 8. Fe Deficiency Anemia: - Oral Iron Salts: - Ferrous forms better absorbed than ferric (ferrous sulfate, ferrous lactate, ferrous fumarate) IV Iron Dextran: - Can cause allergic reactions *Give Iron supplement 2 hours before tetracycline & antacids-bind to iron 9. B12 Deficiency Anemia: - Vitamin B12 (Cobalamin) injection: o Do not expose crystalline injection to light o Do not mix with other drugs in a syringe o IM or deep SQ o Increase Vit. B12 in the diet- liver, eggs, milk, green leafy products 10. Folic Acid Deficiency Anemia: - Vit. B9 supplement o Do not expose injection to light o Do not mix with other drugs in a syringe o Monitor for hypersensitivity o Interaction: Methotrexate, Phenytonin, contraceptives o Teach to avoid alcohol and tobacco o Increase Vit. B9 in the diet sources-leafy green veggies, oatmeal, peanut butter 11. Aplastic Anemia: - Blood transfusion, bone marrow transplant, immunosuppressive therapy o Oxygenation, bleeding precaution, infection prevention 12. Sick Cell Anemia: - Folic acid supplementation, blood transfusions, genetic counseling o Hydration, Oxygen, Rest, Pain management

13. Hematopoietic Stimulants: - Epoetin Alfa (Procrit & Epogen) & Darbepoetin Alfa (Aranesp) o Synthetic formation of erythropoietin Indications: Anemia caused by several conditions Myelosuppressive anticancer chemotherapy Chronic Renal Failure Used to raise Hgb and reduce the need for BT Administer IV or SubQ o Epogen Alfa (Procrit & Epogen) Half-life: 4-13 hours peak within 24 hours (IV) peak 5-24 hours o Darbepoetin Alfa (Aranest) Half-life is 49 hours-long term o Adverse Effects May make client feel no better than before administration Bone pain-working hard Hypersensitivity Risk of tumor progression in cancer patients HTN Thromboembolism-stroke o Nursing Implications Advise prescriber if the patients Hgb is 12 g/dl or better-stop Assure that there is adequate iron, B9 & B12 in the diet Advise patient about Side Effects Must be refrigerated 14. Neutropenia & Immunostimulants: - Colony Stimulating Factors: synthetic formulation of cytokines used to stimulate production of WBC thus reducing the risk and severity of infection in neutropenic patients. o Drug Formulations: Granulocyte colony-stimulating factor (G-CSF) o Filgastim (Neupogen) & Pegfilgastim (Neulasta) Granulocyte-macrophage colony-stimulating factor (GM-CSF) o Sagramostim (Leukine) Administer IV or Sub Q Must be refrigerated Stopped when WBC normalizes o Indications: Chemotherapy-induced neutropenia Bone marrow transplant (will take 2-4 weeks to mature) G-CSF-can be used to collect stem cell GM-CSF- used to promote arterioles in IHD (promote angiogenesis) o Nursing Implications: Remove from refrigerator 30 minutes before injection. Do not shake the medication. Teach patient about common side effects: Bone Pain

Tenderness at the site of injection Blood test abnormalities (temporary elevation in lactate dehydrogenase, and alkaline phosphatase). These will return to normal once treatment is discontinued.

15. Thrombocytopenia: ITP - Steroids & Immunosuppressants Plasmapharesis for removal of autoantibodies - Transfusion of platelets - Splenectomy: last resort TTP - Plasmapharesis for removal of large vWF - Cryosupernatant plasma & Solvent-detergent plasma for TTP - Contains no vWF - Do NOT transfuse platelets with TTP! o Adding fuel to the fire o Unless life threatening bleeding is present o MI and strokes have reportedly occurred after transfusion HIT - NO heparin and heparin products - Argatroban, Lepirudin, Fondaparinux (Arixtra) for antithrombotic prophylaxis to patients with history of HIT 16. Cancer: Chemotherapy: - Use of antineoplastic drugs to promote tumor cell death, by interfering with cellular function and reproduction o Cell Cycle Nonspecific: Useful against tumors that have a low percentage of replicating cells Generally have more toxicity in cycling cells *More adverse effects than cell cycle specific Attack anything, any stage o Alkylating Agents Action: Alkylation of DNA is the crucial cytotoxic reaction that is lethal to the tumor cells (Destroy DNA of cancer cells) Do not discriminate between cycling and resting cells Nitrogen Mustard (Mechlorethamine HCl), Cisplatin, Cyclophosphamide, Nitrosureas (Carmustine, Lamustine, Semustine) Toxic Effects: reversible renal tubular necrosis, hemorrhagic cystitis, mutagenic and carcinogenic. Can damage own DNA when touching it. o Anti-tumor Antibiotics Action: owe their cytotoxic action primarily to their interactions with DNA, leading to disruption of DNA function. Damage DNA of cancer cells at any stage. In addition to intercalation, they have the ability to produce free radicals also play a major role in their cytotoxic effect. They are cell cycle nonspecific.

Examples: o Actinomycin D, Bleomycin, Adriamycin (Doxorubicin) Toxic Effect: Damage to cardiac muscle, pulmonary fibrosis

Cell Cycle Specific Chemotherapeutic agents that are effective only against replicating cells-that is, those cells that are cycling Harsher, S or M phase normally Affects rapidly dividing cells more: bone, hair, mucous membranes Anemia, Increased risk of bleeding, increased risk for infection o Antimetabolites Action: structurally related to normal compounds that exist within the cell. Block DNA replication. S-phase. Interfere with the availability of normal purine or pyrimidine nucleotide precursors by inhibiting their synthesis Competing with them in DNA or RNA synthesis Their maximal cytotoxic effects are in S phase (and therefore, cell cycle specific) DNA cant replicate and die. o Examples: Methotrexate-Blocks B9 synthesis Folic Acid deficiency anemia-macrocytic 5 fluorouracil 6 mercaptopurine o Toxic Effects: Nausea, vomiting, stamatitis, diarrhea, alopecia, bone marrow suppression Leucovorin Rescue: Ability to protect normal cells to have normal metabolites, given after increased dose of methotrexate Mitotic Inhibitors Action: Prevent cell division during M phase of cell division The mitotic spindle consists of chromatin plus a system of microtubules composed of the protein tubulin The mitotic spindle is essential for the equal partitioning of DNA when a eukaryotic cell divides. (Prevent microtubules) Examples: o Vincristine, Vinblastine o Structurally related compounds derived from the periwinkle plant, Vinca rosea (vinca alkaloids) o Binds to the microtubular protein, tubulin o Blocks the ability of tubulin to polymerize to form microtubules Toxic Effects: Alopecia, bone marrow suppression, peripheral neuropathy, affects neurotransmission

Hormones - Tumors that are steroid hormone-sensitive may be either: o Hormone responsive- Tumor regresses following treatment with a specific hormone o Hormone dependent- removal of a hormonal stimulus causes tumor regression Tamoxifen (Novaldex) Estrogen antagonist Used for first line therapy in the treatment of estrogen receptor-positive breast cancer Flutamide, Nilutamide, and Bicalutamide Synthetic, nonsteroidal antiandrogens used in the treatment of prostate cancer Immunotherapy - Monoclonal Antibodies o They are created from B lymphocytes (from immunized mice or hamsters) fused with immortal Blymphocyte tumor cells. o Cloned to produce antibodies directed against a single antigen type. o Several monoclonal antibodies are available Trastuzmab, Rituximab, Bevacizmab, and Cetuximab - BCG (Bacillus-Calmette & Guerin) o Injected directly into solid tumor o If exposed to TB o How will this kill tumor cells? Immune system attacks cancer cells *Know Chemo Man!! Cell Cycle Non-Specific Alkylating Agents Antibiotics Cisplatin Nitrosureas Effective for both low-growth fraction malignancies (Solid-tumors) as well as high growth fraction malignancies. Slow growing

Cell Cycle Specific Antimetabolites Bleomycin antibiotics Vinca alkaloids Etoposide Effective for high growth fraction malignancies (hematologic cancers) Rapidly growing

Disease
Emphysema (COPD) Destruction of alveolar walls Decreases surface area available for exchange. Increased resistance to pulmonary blood flow Difficulty in exhalation caused by airway obstructed by edema or excessive mucus production Lung hyperinflation due to air trapping Increased work of breathing

Etiology/Risk Factors
Cigarette smoking is the primary etiology Chronic respiratory inflammation from pollution or occupational substances are contributory factors Diagnosis in young and middle age adult with no history of smoking maybe associated with hereditary deficiency in alpha-1 antitrypsin-which breaks down elastin more quickly, less elasticity in alveoli.

Assessment
Pink Puffers (oxygenated fine) Barrel Chest, obvious use of accessory muscles, pursed lips (prolonged expiration becomes an active process), underweight appearance -not eating much, increase in metabolic demand b/c of WOB. Tripod position Cough mostly in AM Persistent tachycardia Dyspnea on exertion with advancing disease Enlarged accessory muscles Clubbing of fingers (decreased oxygen) with disease progression Diminished breath sounds & wheezing or crackles may be present on auscultation

Symptoms
Barrel Chest Pursed lips Underweight Tripod Cough Tachycardia Dyspnea Clubbing of fingers

Lab/Diagnostic Tests
ABG: slightly decreased PaO2. PCO2 is low during early stages of the disease (breathing fasterrespiratory alkalosis) and elevated on later stages, diminished PaO2 (hypoxia) is the drive to breathe in later stages. lead to CO2 retainers. PFT (Pulmonary Function Test): low vital capacity (VC) and forced expiratory volume, increased residual capacity CBC: possible polycythemia (many RBCs) in later stages. Increased oxygen demand (more carrying capacity) CXR: barrel chest, flattened diaphragm on CXR Serum-alpha 1 Antitrypsin

Complications
Increased risk for pulmonary infectionPneumonia Can lead to pulmonary hypertension (more blood flow) Cor pulmonale- right sided heart failure. Pumping makes right side bigger, works harder. Dysrhythmias Cancer

Medications/Treatment
Goal of Management: Correct hypoxia Reverse bronchospasm Treat inflammation Supportive Bronchodilators: open the airway to reduce dyspnea and increase FEV 1) Adrenergic agonist (B2 agnosist) Mimics sympathetic nervous system. Short acting-used for acute episodes of asthma Albuterol, Bitolerol, Pirbuterol, and Terbutaline Long acting: used for prevention of acute attack Formeterol, Salmeterol 2) Anticholinergic agents Parasympathetic, blocks PSNS thus preventing bronchoconstriction, decreases the production of secretionincreased heart rate, constipation, nausea, urinary retention Atropine, ipatropium (Atrovent), Tiotropium Bromide (Spiriva) 3) Methylxanthines Directly relaxes smooth muscles of the bronchial treebronchodilation Aminophylline (Theophylline) Anti-inflammation: 1) Steroids Administer steroids to decrease inflammation within the airways IV: Hydrocortisone, methylprednisolone PO: Prednisolone, prednisone Inhalers: Beclomethasone, Triamcinolone, Fluticasone, Budenoside, Flunisolide inhalers

Chronic Bronchitis (COPD)

Disease of chronic airway inflammation & increase bronchial secretion Cough lasting 3 months or more in 2 consecutive years Chronic inflammation of the airway causes hyperplasia of mucus glands Goblet cells develop in abnormal sites in terminal bronchioles Cilia disappears and their clearance function is lost Mucosal edema and increased mucus progressively obstructs airway. Inflammation, decreased cilia, increased mucus, cant move-cough

Cigarette smoking is the primary etiology Chronic respiratory inflammation from pollution or occupational substances are contributory factors

Blue Bloaters Cyanosis, increased tendency for obesity Cor pulmonale Frequent productive cough (during winter, foul smelling) Wheezing & Rhonchi may be present Tachycardia Tachypnea with use of accessory muscles Frequent pulmonary infection Fever in acute episode due to infection

Cyanosis Obesity- hypoxicdecreased activity, increased heart rate and respirations Cough Wheezing & Rhonchi Tachycardia Tachypnea Fever in acute episodes

ABG: slightly decreased PO2, PCO2 is low during early stages of disease and elevated later stages, diminished PaO2 (hypoxia) is the drive to breath in later stages alkalosis acidosis Constant Increased CO2 = decreased sensitivity (drive to breathe decreases), when O2 decreases = breathe

Asthma Phase 1: release of histamine, prostaglandins, and leukotrienes Bronchoconstriction Bronchial edema Increased mucus production Phase 2: WBC invades bronchioles, causes edema and swelling of bronchioles, tissue damage

Intrinsic etiology: Uncertain causes: physical & psychological stress; exercise induced Extrinsic etiology: Antigen-antibody reaction to specific irritants/triggers Dust, dander Chemicals (smoke, smog) Respiratory infections Cold and dry air Hormonal influences Medications (aspirin, NSAIDs) Food additives

Severe SOB Expiratory wheezes Cough Feeling of chest tightness Prolonged expiration Tachypnea with use of accessory muscles Tachycardia Diminished or absent breath sounds (increased secretions)-maybe related to atelectasis or pneumothroax Extreme restlessness, anxiety and agitation Intercostal retractions Use of accessory muscles Hyper-resonant sound on percussion (airway decreased, increased secretions)

SOB Wheezing Cough Chest tightness Long expiration Tachypnea Tachycardia Diminished or absent breath sounds Restlessness Intercostals retractions Hyper resonance

ABG: decreased PO2, mild respiratory alkalosis during initial attack, respiratory acidosis with disease progression CBC: elevated Eosinophils count during episodes or attack Charcot-Leyden sputum PFT (Pulmonary Function Test): decreased vital capacity (VC), forced expiratory volume (FEV1) & peak expiratory flow rate, increased residual capacity Used to evaluate the degree of airway obstruction Done before and after use of aerosol bronchodilators to determine the reversibility of airway obstruction Decreased FEV or peak expiratory rate flow (PERF) during attack

Status Asthmaticus: severe, prolonged asthma attack which cannot be broken by usual treatment Wheezing may be absent Silent chest Severe acidosis May have to intubate Early: alkalosis, and good O2. Late: acidosis

Leukotriene Inhibitor/Modifiers Suppress inflammatory process by blocking a group of inflammatory mediator called Leukotrienes Montelukast (Singulair), Zafirlukast (Accolate), Zileuton (Zyflo) 3) Mast Cell Stabilizers Mast cell stabilizer can retain an early component of the initial response to allergens which will prevent reaction from occurring Treatment prior to allergen exposure or help prevent attacks Cromolyn sodium Other: Administer expectorants Guiafenesin (Mucinex) Administer Alpha 1-antitrypsin therapy for patients with deficiency Administer Antacids, H2 Blockers, or proton pump inhibitor Administer diuretics if patient develops RHF Furosemide, Bumetanide Administer Vaccines Pneumonia Flu (may precipitate asthma attack)

2)

Nursing Diagnosis: ineffective airway clearance. Ineffective breathing pattern. Risk for infection. Imbalanced nutrition less than body requirements. with advanced COPD, minimal activity can cause fatigue including eating. Anxiety, decisional conflict: smoking

Ineffective airway clearance & ineffective breathing pattern: monitor VS for compromised respiratory status every 2 hours. Monitor skin color and LOC. Assess ABG. Monitor O2 satcheck H&H too! Monitor sputum for color, amount, semi-fowlers. O2 @ 2L/min. Rest. Increase OFI 20002500ml & monitor I&O. Chest physiotherapy. Medications. Suction.

Imbalanced nutrition less than body requirements: assess nutrition status, diet, height and weight, anthropometric measurements. Document food intake. Monitor albumin & electrolytes. Refer to dietician. Provide small frequent feedings. Increase protein & calories. Upright position. Bring food from home.

Decisional Conflict: Smoking: assess knowledge and understanding of the choices involved. Acknowledge concerns, values, beliefs, help plan course of action for quitting, respect patients decision, referralcounselors, professional, and self-help groups.

Community Based Care: avoid triggers: indoor exercise during cold season, warm up slowly prior to swimming, decrease stress, meds. Reduce risk of infection: flu vaccine, pneumonia vaccine for elderly. Explain: peak flow meter, metered dose inhaler, dry powder inhaler, recognize early sign of asthma

Peak Flow Meter: Peak expiratory flow rate: reading done at varying time of the day to establish patients baseline. Green: 80-100% Yellow: 50-80% Red: 50% or less-need bronchodilator and medical treatment if yellow

Turning, Incentive S. Pleural Effusion Accumulation of fluid in the pleural space Disease/abnormality Transudate: Fluid contains some protein Fluid moves from capillaries to the pleural space Increases hydrostatic pressure Decreases oncotic pressure Exudate: contains large amount of protein. Inflammation causes increased capillary permeability. Exudation brought about by pulmonary infection. Obstruction of mediastinal lymphatics Empyema Pleural fluid containing pus Associated with infectious process: pneumonia, tuberculosis, lung abscess Chylothorax Disruption of pulmonary lymph: surgery, trauma Produces fat malabsorption from GI tract -impaired lymphatic drainage leads to increased pressure and leakage of lymph into the intestinal lumen. The impairment of chlyomicron and lipoprotein absorption. Results in malabsorption of fats and protein. Carbohydrates are not absorbed

Swimming is good. Visible on chest xray if more than 250 ml of fluid accumulates Diagnostic thoracentesis: differentiate source of pleural fluid Thoracentesis: Xray or US is used to locate the effusion. A thin, hollow plastic tube through the thorax, a syringe is attached to draw fluid out of your chest. This procedure can remove 1200-1500 ml of fluid at a time because of cardiovascular collapse as a risk. Treatment of choice especially if dyspnea is present Pre-procedure: may or may not require NPO, sedation is Not required, cough suppressant if needed, prepare equipment-sterile, orhtopneic positionopens spaces for better needle insertion, may feel pressure Post: monitor VS during procedure, apply dressing and position patient on unaffected side for 1 hour. Assess for bleeding post procedure, Obtain CXR post procedure-resume normal activities after 1 hour if no pneumthorax, send fluid to lab Abrupt onset Pleuritic Chest Pain Dyspnea Tachypnea Decreased Breath Sounds on affected side Assymmetrical chest movement
Spontaneous pneumothorax: in otherwise healthy client resolve without invasive treatment. For recurrent spontaneous pneumothorax, pleurodesis may be indicated.

Goal is to treat the underlying cause: Thoracentesis, antibiotic therapy, surgical repair-pleurodesis, pharmacotherapy: analgesics, antipyretic, IV lipids if chylothorax is present Monitor respiratory and oxygenation status, provide supplemental oxygen if indicated, provide adequate nutrition with focus on protein intake, explain the underlying cause, instruct about purpose of throacentesis/thoracostomy Throacostomy: remove fluid, air, or blood from the pleural space. For larger amounts of fluid, a chest tube is indicated. A chest tube also is needed to drain blood and air from pleural space

Pneumothorax/Hemothorax
Air accumulation in the pleural space Spontaneous* 1) Simple or closed pneumothroax Rupture of air bleb allows pathway of air movement between respiratory system and pleural space Collapse of involved lung tissue

NO OPENING Lung collapse from air bleb

If pressure between thoracic cavity and atmosphere equalizes, chest will become symptomatic. No opening in chest wall.

2) Tension pneumothorax Air leaks through lung or chest wall. Air builds in pleural space with no where for the air to escape. One way valve results in collapse of lung on affected side. Results in pressure on mediastinum, the other lung and great vessels. Mediastinum shifts to opposite side, inferior vena cava kinks on diaphragm leading to decreased venous return and cardiovascular changes 3) Traumatic or Open Disruption of the pleura, bronchi or lung tissue cause by blunt or penetrating trauma with air accumulation in pleural space Opening in chest cavity that allows air to enter pleural cavity. Causes the lung to collapse due to increased pressure in pleural cavity Can be life threatening and can deteriorate quickly

Hyperresonance on affected side because it is air filled Anxiety/Restlessness Severe dyspnea Absent breath sounds on affected side Tachypnea Tachycardia Poor color Accessory muscles use JVD Narrowing pulse pressure Hypotension Tracheal deviation (late)

In mild cases, no chest tube is required; if the pneumothorax is significant, a chest tube is inserted.

For TENSION pneumothorax: One way-valve (Heimlich valve) -For emergency treatment of tension pneumothorax -Catheter over needle is inserted in the 2nd intercostals space -Catheter remains in chest after needle is removed. -audible hissing sound confirms presence of tension pneumothroax -Procedure creates a simple pneumothorax

Dyspnea For OPEN pneumothorax, seal Sudden sharp pain defect and secure only on 3 sides. Subcutaneous Placement of chest tube with emphysema Absent lung sounds on water seal drainage. affected side Red bubbles on exhalation from wound Asymmetrical chest movement Decreased respiratory excursion Hemothroax Anxiety/restlessness CXR reveals Signs of shock pneumothorax or Occurs when the pleural space fills Frothy bloody sputum hemothorax ABG shows with blood. Usually occurs due to decreased PaO2. Absent breath sounds on lacerated blood vessel in throax. As affected side blood increases, it puts pressure on Cyanosis heart and other vessels in chest Dullness on percussion of affected side cavity. Each lung can hold 1.5 liters Flat neck veins of blood (decreased blood) Collaborative care: impaired gas exchange, ineffective breathing pattern, decreased cardiac output, pain, anxiety Monitor respiratory and oxygen status. Provide supplemental oxygen as indicated. Maintain infection control. Provide antibiotic as ordered. Provide analgesics for pain control. Teach purpose of chest tube. Teach about activity limitations. Care for chest tube. Chest tube: The purpose of a chest tube is to reestablish negative intrathoracic pressure following equalization of pressure between chest and atmosphere due to: pneumothorax/hemothorax, pleural effusion, trauma, surgery (drain blood from the mediastinum after open-heart surgery) Chest drainage system: -Drainage or collection chamber: collects drain, can be marked per shift or more frequently to tract amount of output. -Water seal chamber: prevent air and drain from flowing back into chest. Tidaling observed with patient breathing. Occasional bubbling is normal. -Suction control chamber: helps reestablish the negative pressure. Connected to suction. Nursing interventions: place patient in semi-fowlers position. Monitor vital signs for changes every 4 hours. Monitor O2 Saturation and ABGs. Monitor respiratory rate, effort, use of accessory muscles, skin color and breath sounds. Monitor respiratory status: pneumothorax can enlarge or reoccur even in the presence of a patent chest tube drainage system. Teach importance of turning and DBCE. Control pain. Care of chest drain: Maintain occlusive dressing. Check tubing frequently for kinks and loops. Milk chest tube to maintain patency only if ordered. Keep collection apparatus below the chest. Maintain the indicated amount of water in water seal chamber. Below normal water creates higher suction causing pleural tissue damage. Monitor drainage of chest tube for the amount and characteristics of output every 8 hours. More than 70 ml per

hour, red warm and free flowing drainage, cloudy output. No continuous bubbling should be noted (occasional bubble may be normal) in the water seal chamber-indicates a leak. Water level should fluctuate with respiratory efforts. Apply sterile occlusive petroleum jelly dressing post removal of chest tube (x-ray) post insertion and post removal.

Disease
Pneumonia Inflammation of lung parachyma 7th leading cause of death in US leading cause of death from infectious disease. 10% of all adult hospitalizations. Problem especially for older adults and those with debilitating disease.

Etiology/Risk Factors
Causes: Infectious: bacteria, viruses, fungi, protozoa Noninfectious: aspiration of gastric contents, toxic gases Most common organism for community acquired = Streptococcus Pneumoniae (50%); gram + Nosocomial = Staph, E coli, Klebsiella Inhaled; migrated to alveoli; inflammation Infectious debris and exudates fill alveloli; consolidation; impaired gas exchange

Assessment

Symptoms

Lab/Diagnostic Tests
Sputum Gram Stain: done initially; determines whether organism gram positive or gram negative (minutes to find out) Antibiotic initiated based on predominant type of organism Sputum Culture: identify actual infecting organism Determine the appropriate antibiotic therapy Procedure: done before any antibiotic started; first rinse mouth with water; early AM; cough deeply. Sputum in morning before antibiotics. No toothpaste/brushing Get nebulizer 1st. WBC Count: Acute bacterial pneumonia-WBC elevates (15-20,000 common). Minimal WBC changes with viral. Shift to left (High # immature leukocytes = bands) Chest XRAY: extent of lung involvement; fluid and infiltrates = densities

Complications/Additional Medications/Treatment information

Prevention: Encourage influenza vaccines yearly (especially for those at risk); vaccine not for those with egg allergies or those who previously reacted. Pneumococcal vaccine usually permanent immunity with single dose. Living longer-need second dose. One time revaccination for those at great risk. Bronchoscopy: lighted scope inserted through mouth and larynx into tracheobronchial tree. Direct visualization tissues and specimen collected Nursing care pre-procedure: requires informed consent, NPO after MN or 6-8 hours before procedure. Pre-meds: sedation, local anesthesia Post procedure: No fluids/food for 2 hours until cough and gag reflex return. Monitor color and character of secretions. Normal for bloody secretions for several hours. Notify MD: Grossly blood secretions; persistent cough; wheezing, SOB, chest pain. Hoarseness-warm saline gargles, throat lozenges may help; mild fever is common in first 24 hours. Whisper for 1st day. Antibiotics: after gram stain results and x-ray results show pneumonia process. Broad spectrum initially (clarithromycin, azithromycin, or erythromycin) a PCN or cephalosporin, or Cipro Narrow spectrum after culture result is noted. Bronchodilators: (if bronchoconstriction or spasm) Sympathomimetics (bronchodilation) Albuterol/Proventil; Alupent Methylxanthines (bronchodilation) Theophylline/Aminophylline Antipyretics Tylenol 650 mg po q 4 for temp > 101 Liquefying Agents: Mucomyst, Guaifenesin Complementary therapy: Echinacea- herb that stimulates immune function. dont take with autoimmune disorder. Will increase immunity.

1)

Acute Bacterial

Streptococcus Pneumoniae

Very sick episode with this type of pneumonia. Generally resolves without residual lung changes. Organism usually is Streptococcus Pneumoniae More mild than bacterial Community outbreaks generally viral.

2)

Viral walking pneumonia

10% of pneumonias Organisms= influenza & adenovirus

Rapid onset Shaking chills, fever, cough Rust colored or purulent sputum Pleuritic chest pain (hurts to breathe in) Decreased breath sounds or crackles HA Fatigue Malaise

3)

Fungal

Organism multiplies outside alveoli in the alveolar septum & intestinal spaces of lungs Histoplasmosishistoplasma capsulatum (bird poop)

Dry cough Muscle aches Amphotericin B-very potent -Often a serious acute reaction after the infusion (1 to 3 hours later) is noted consisting of high fever, shaking chills, hypotension, anorexia, nausea, vomiting, headache, dyspnea and tachypnea, drowsiness, generalized weakness. *Nephrotoxic Itraconazole & Corticosteroids Fever of abrupt onset Tachypnea with SOB Dry non-productive cough Significant resp distress; requires ventilator

4)

Pneumocytis Carinii Pneumonia (PCP)

75-80% of those with AIDS develop (opportunistic) Also develops with immunosuppressive therapies Gastric contents move into lungs. Those at risk: depressed cough, impaired swallowing; NG or G tube feedings; older adults, altered LOC, emergency surgery Lungs receive acidic fluid, set up inflammatory response; numerous cells; edema; eventually resp failure, gangrene of tissue

5)

Aspiration Pneumonia

Oxygen Therapy:
Low flow systems: Nasal Cannula Low flow, low concentrations Delivers 24-45% O2 concentrations Flow rate 2-6 L/min Good for COPD clients Simple Face Mask Low flow but moderate concentrations Delivers 40-60% O2 concentrations (Cannot deliver <40% O2) Flow rates 5-8 L/min Non-rebreather mask Low flow but high concentrations Delivers up to 100% O2 (usually 60-90%) Highest amount possible without ventilator Partial rebreather mask Low flow O2 reservoir bag attached; possible to deliver high O2 concentration High Flow system:

Venturi mask Allows for precise regulation of O2 24-50% O2 Regulates ratio O2 to room air

Chest Physiotherapy: Includes 3 Processes: 1) Percussion: rhythmically strike/clap chest with cupped hands; loosens secretions; never done on bare skin, sternum, kidneys, spine or breast tissue; produce hollow sound; can be done mechanically. 2) Vibration: used with percussion but can be used when percussion not tolerated; moves secretions into larger airways; repeatedly tense the arm and hand muscles while maintaining firm but gentle pressure over area with flat of hand 3) Postural drainage: positioning, use of gravity to facilitate secretion removal; done after bronchodilators given; done before meals. Ineffective Airway Clearance: Check vitals and breath sounds at least q 4 hours. Note cough and sputum production. Monitor ABGs as ordered. Changes are early indicator of imp. Gas exchange. Want O2 > 80 mmHg and CO2 <45 mmHg. Fowlers position. Hydration (2500-3000 ml) liquefies secretions but also if fever will prevent dehydration. Administer as ordered O2, CPT, SaO2 (want > 92%), antibiotics, bronchodilators. Incentive spirometer to promote coughing/deep breathing. DBCE, CPT-mobilize secretions. Note LOC-irritability and restlessness prime signs of cerebral hypoxia. Suction as ordered, Remember never suction > 10 seconds; only pass catheter 3 times; best to oxygenate prior. Ineffective Breathing Pattern: Assess respiratory rate and depth; lung sounds Louder breath sounds heard over areas of consolidation-sound waves easily transmitted over consolidated tissue. May develop pleuritis. Analgesics for pleuritic pain. Teach abdominal breathing. Promotes lung expansion, relaxation techniques. Activity Intolerance: Assist with self care. Scheduled rest periods. Bedrest during acute phase (fever, elevated WBCs) increase activity when WBC more normal and Afebrile. Well balanced diet hi calorie. Small meals, raise head of bed during meals to prevent risk of aspiration and further problems. Position on side after meals not on back.

Disease
Tuberculosis TB is an ancient infectious disease caused by Mycobacterium tuberculosis. It has been known since 1000 BC. Declined steadily till mid 1980s attributed to improved sanitation, surveillance, and treatment. Opportunistic disease

Etiology/Risk Factors
Mycobacterium tuberculosis -Increased incidence of AIDs -Multiple Drug Resistant (MDR) strains -Migration, poverty, homelessness, drug abuse. Since TB is transmitted via droplet nuclei optimal conditions for transmission include: -overcrowding, poor personal hygiene, poor public hygiene Patients with the active disease (bacilli) may expel them into the air by: -coughing, sneezing, shouting

Assessment
Pathogenesis: Caused by mycobacterium tuberculosis. -Once inhaled the bacilli multiply 4-6 weeks. Commonly in the lung but may also spread in other parts of the body with high partial pressure of oxygen: lung, kidneys and ureters, bones, CNS. The immune system fights the infection forming scar tissue around the TB bacteria called Ghon Complex. The infection is contained in an inactive/dormant state as long as immune system remains active. Typically has no symptoms and cannot spread TB to other people. XRAY: looks like spots on lungs. TB that occurs after initial

Symptoms
Reactivation TB: -occurs when a persons immune system is depressed. Local or systemic spread. Vein-via left ventricle to whole body. Artery- miliary spread within the lung (miliary tb) Fatigue, anorexia, weight loss, night sweats and afternoon fever, dry to productive cough, hemoptysis and pleuritic pain, progressive dyspnea, multiple lesion on XRay Extra-pulmonary TB: Pott Disease

Lab/Diagnostic Tests
Early Detection: PPD (Mantoux test) shows exposure to tuberculosis. Positive after 3-10 weeks from exposure. Intradermal 0.1 ml of PPD at dorsal aspect of forearm. Weal formation. Read after 48-72 hours, induration size. Shows exposure, develop antibodies. **Look at screening slides on pwrpt. Accurate Diagnosis: Acid Fast Bacilli (AFB) for diagnosis and evaluation. 3 negative smears to assure low infectivity. Culture most sensitive and specific test.

Complications/Additional Medications/Treatment Information

Prophylaxis: if exposure to persons with active disease, but has no clinical evidence of disease. INH for 6 months. Bacillus Calmette-Guerin (BCG) -In US BCG is required in infant, children and healthcare workers who have negative PPD but are recurrently exposed to people with active TB. Goal of drugs: make the disease noncommunicable to others. Reduces symptoms of disease. Effect a cure in the shortest possible time. Additional Drugs: Active TB w/ HIV: treatment for minimum of 9 months. Rifampin interacts with Protease inhibitors. -Rifabutin & Rifapentine Drug Interaction: competition between Isoniazid and Phenytoin (anticonvulsant). They both compete for drug metabolism enzymes. Phenytoin interferes with metabolism

Prior to starting Antituberculosis Drug Therapy: liver function test, vision exam, renal panel, audiometric testing. Let us know if there is a change in sight or hearing. No alcohol or acetaminophen. Minimum treatment is 6 months. Short Course Chemotherapy (SCC): INH, Rifampin (Rifadin), Pyrazinamide (Tebrazid), and ethambutol (Myambutal) given daily or 2-3 times weekly. For 2 months then AFB & CXR

-if AFB &CXR are negative-continue INH & Rifampin for 4 months (total of 6 months). -if AFB & CXR are positive- continue INH and Rifampin for 2 months then sputum culture. --if culture is negative-continue INH and Rifampin for 2 months (total of 6 months).

exposure to the bacteria referred to as primary TB.

***KNOW MED SLIDE ON PWRPT Effective Disease Treatment: Sputum Culture and CXR are used to evaluate treatment post SCC treatment. 3 negative sputum culture means the patient is cured. Usually negative sputum culture after 2 months of therapy. Positive sputum culture beyond 3 months suggests treatment failure or drug resistance. Organism needs to be tested for susceptibility to anti-tubercular drug. Sputum negative = good. 3 consecutive negative to have non-active TB. Prevention of Spread: Private room-NEGATIVE pressure room. Covering mouth when coughing or sneezing. Teach strict compliance with treatment. Place mask on the patient when being transported to other parts of the hospital. Visitors should wear specially fitted air mask (N95 respirator) when entering room. Respiratory isolation (airborne precautions). Neg = nurse protection hallway air into room. Reverse Isolation: Laminar/Negative pressure room. Air is sucked in from the hall into the room. Air is then filtered. Purpose is to prevent disease from escaping from the patients room. Priority Nursing Diagnoses: ineffective breathing pattern, ineffective health maintenance, imbalanced nutrition: less than required, hyperthermia, pain, activity intolerance, isolation Interventions: monitor respiratory rate, effort and use of accessory muscles & skin color changes. Increase oral fluid intake if not contraindicated, record I& O, promote rest, good nutrition-B9, B6, protein, vitamin C, eccanasia. Implement infection prevention measures. Assess for medication side effects. Client education: infection control measures, mechanism of transmission-droplet, adverse effects of medication, need for good nutrition and adequate rest, reduce secondary infection, adequate hydration, avoid alcohol and smoking, teach to cover mouth and nose when coughing. Expected Outcomes: adherence to medication regimen, resolution of productive cough, Afebrile, respiratory rate WNL, pulse oximetry WNL, maintenance of normal body weight, resolution of infection, prevention of spread of infection.

Chest Xray- for diagnosis and evaluation.

of isoniazid by reduction in excretion or enhancement of effect of isoniazid.

--If culture is positive-continue INH and Rifampin for 5 months (total of 9 months)

Disease
Pulmonary Embolism

Etiology/Risk Factors
Clots: typically caused by 3 factors: hypercoagulable state, vessel trauma, venous stasis -Manifestations will depend upon where the thrombus occurs and/or where the emboli becomes trapped in the vasculature.

Assessment
PE may result in: Increased alveolar dead space-no perfusion, hyperventilation, hypoxia and hypoxemia, pulmonary infarction (later, uncommon)decreased profusion to lunglung dies. Ventilation-perfusion mismatch

Symptoms
Hemodynamic effects: increased pulmonary resistance. Increased RV afterload. RV failure may ensue. Occlusion of Large Pulmonary artery resulting in sudden death. Dyspnea, anxiety and apprehension, feeling of impending doom, tachycardia and tachypnea, cough, diaphoresis, low grade fever-clotting cascade response

Lab/Diagnostic Tests
ABG: hypoxemia (PaO2 <80). Hypocapnia and respiratory alkalosis acidosis Color-flow Doppler Imaging: for DVTs (if positive start anticoagulation) Pulmonary angiography: contrast medium injected into the pulmonary artery Spiral CT: it visualizes main, lobar & segmental pulmonary emboli FDP (fibrin degradation products) & D-Dimers: are the by-products of fibrin breakdown. Indicates there are/were clots that are being dissolved. D-dimer is one type of FDP V/Q scan: radiogated albumin is injected in IV and is distributed in the lungs. Then lungs are scanned for distribution of the radio-isotope. Watch flow in lungs. Radiotagged gas are inhaled and lungs are scanned for gas distribution.

Complications/Additional Medications/Treatment Information

Coagulation Studies: PTT: intrinsic clotting pathwayHeparin- 1.5-2 times the controlled value. PT/INR: extrinsic clotting pathwayWarfarin- therapeutic range- 2-3. Allowed to take aspirin. Can take all three. **Understand chart of Warfarin and heparin Heparin: dose is adjusted to maintain an aPTT in the therapeutic range (upper limit of normal). Arixtra if have HIT. Warfarin: effect occurs after 3672 hours. 5-7 days to be fully effective. The recommended therapeutic range for venous thromboembolism is an INR of 2-3. Once the patient is stabilized on a specific dose, the INR may be checked every 1-2 weeks. dont eat green leafy vegetables. Vitamin K.

Anticoagulation therapy: RISK FOR BLEEDING. Prepare antidote. Heparin-Protamine sulfate; Coumadin-Vitamin K. Increase risk for bleeding is higher when: Cardiac, liver or renal disease. Age over 60. Thrombolytic therapy: accepted indications include (hemodynamic instability, RV dysfunction on echocardiography) contraindications: intracranial disease, recent CVA, active bleeding, bleeding disorder, pregnancy, HTN severe, recent surgery or trauma. **Know the Fibrinolysis cascade. Prevention: active/passive ROM exercise. External pneumatic compression device. Antithrombotic stockings. Early ambulation. Anticoagulants-porcine heparin, enoxaparin (lovenox), fondapannux (arixtra) Acute Episode: oxygen, bed rest, analgesic to control pain and decrease myocardial oxygen demand. Administer anticoagulant or fibrinolytic agent as ordered. Pulmonary artery wedge pressure monitoring (Swan-Ganz). IVC filter (Greenfield Filter): Indicated if: absolute contraindication to anticoagulation. Recurrent venous thromboembolism despite adequate anticoagulation. Impaired Gas exchange: Assess respiration, high flow O2 and monitor ABG. Semi-fowlers position. Bed rest. Decreased cardiac output: assess VS, assess skin color, monitor cardiac rhythm, administer pressors as ordered (ICU setting), monitor neck vein distention & peripheral edema. Ineffective Protection: bleeding precaution, monitor coagulation studies-PTT & INR , prepare antidote, adequate fluids and stool softeners, avoid invasive procedures, maintain firm pressure on injection and venipuncture sites- 30 mins for arterial puncture. Anxiety: remain with the client as much as possible. Allow supportive family member to stay with patient. Morphine as prescribed (vasodilator), reduce environment stimuli and use a calm reassuring manner. Teach prevention: early ambulation pre-op, antithrombotic stockings, sequential compression device, avoid sitting or standing for long time, avoid crossing legs when sitting, identify site effects from anticoagulation, caution females about the use of hormonal contraceptives and contraceptive pills. **Know how to do Heparin calculations. THE HEART Antilipidemic Agents Used to prevent or slow progression of atherosclerosis to reduce the risk of complications. Goal of cholesterol altering drugs: Individuals without CAD Total cholesterol < 200 mg/dl HDL > 35 mg/dl LDL < 130 mg/dl Individuals with CAD LDL < 100 mg/dl Drugs do not replace need for diet and exercise Lipoproteins Serve as carriers for transporting lipids (cholesterol and triglycerides) in the blood. The composition of blood lipid Cholesteryl esters (CE) Triglycerides (TG) Cholesterol (CH) Phospholipids (PL) Apolipoprotein Major Classes of Lipoprotein Chylomicron VLDL IDL LDL HDL Density is determined by the amount and type of Apolipoprotein embedded in the lipoprotein shell All lipoproteins that deliver lipids to peripheral tissues (nonhepatic tissues) contain apolipoprotein B-100 (Ex: VLDL, LDL) All lipoproteins that transport lipids from peripheral tissues back to the liver contain apolipoprotein A-I (Ex: HDL) Lipoproteins & Atherosclerosis VLDL, IDL, LDL, ApoB VLDL is hydrolyzed into IDL which are converted to LDL LDL Bad cholesterol contains ApoB 100 Removed from plasma via endocytosis by liver converting it to bile acids excreted in GI Makes the greatest contribution to coronary atherosclerosis

Oxidized LDL contributes to atherosclerotic plaque HDL, ApoA Good cholesterol Apo I is cardioprotective Transports cholesterol from the peripheral tissues back to the liver promotes cholesterol removal Antiatherogenic Statins Mode of Action: Examples: Mevacor (Lovastatin) Prevachol (Pravastatin) Zocor (Simvastatin) Lipitor (Atorvastatin) Lescol (Flovastatin) Inhibits hepatic HMG CoA reductase Inhibition of cholesterol synthesis causes hepatocytes to synthesize more LDL receptors Hepatocytes are able to remove more LDLs from the blood

1.

2.

Side Effects: (Fewest adverse effects and tolerated best) HA, rash, GI disturbances (dyspepsia, cramps, flatulence, constipation, abdominal pain) _____________ (report muscle pain/weakness) Hepatotoxic (monitor LFTs) Statins are pregnancy category X - Teratogenic Some other nursing considerations Since LDL cholesterol levels will return to pretreatment values if drugs are withdrawn, treatment must continue lifelong Given at night Niacin (nicotinic acid) Mode of Actions: Decrease VLDL, LDL; Increase HDL Strongly inhibits lipolysis in adipose tissues thus reducing fatty acids Fatty acids are precursor for triacylglycerol synthesis Triacylglycerol needed for VLDL synthesis LDL is derived from VLDL Increases HDL Used in combo with statin drugs Start with low dose and gradually increase Given 1-3g/day in divided doses or once daily with extended release. Give at night with food. Side Effects: Pruritis, rashes, dry skin May cause nausea and abdominal discomfort & PUD Give with meal Flushing face, neck, ears that occurs after drug is started or dose and may last for the first several weeks Diminish flushing by taking 1/2 ASA with dose May cause hypotension May cause Gout Monitor uric acid level

 3.

Hepatotoxic Monitor LFT Can potentially increase blood sugar

Bile Acid Sequestrants Mode of Action: Bile acids, are normally reabsorbed in the jejunum and ileum. When resins are given, they bind to bile acids & prevent their reabsorption excretion creates a demand for synthesis of bile acid. Liver cells must have an cholesterol supply (provided by LDL) to synthesize bile acid. Liver cells will their LDL receptors, ing uptake of LDL from plasma.

Examples: Cholestyramine (Questran) Colestipol (Colestid) Colesevelam (Welchol) Side effects: Constipation Bloating, indigestion, nausea Large doses may impair absorption of fats or fat soluble vitamins (A, D, E, and K) Nursing Considerations: Do NOT give other drugs with Bile acid sequestrants (1 hour before the resin or 4 hours after) Some are dispensed in powder form (must be mixed with fluid). Must be taken with meals

4.

Phenyloxygen acid (Fibrates) Mode of Action: Decrease VLDL thus reducing triglyceride levels Ligand for the nuclear transcription regulator, peroxisome proliferator-activated receptor- (PPAR- ) Examples: Gemfibrozil (Lopid) Finofibrate (Tricor) Clofibrate (Atromid-S) Side Effects: Transient GI disturbances Given with food Billiary stone due to increased billiary cholesterol concentration Use with caution in pts with biliary tract disease, women, obese pts, and Native Americans Myopathy and rhabdomyolysis Report muscle pain/weakness Hypokalemia Monitor for arrhythmia Hepatotoxic Interaction: Transiently potentiating anticoagulant activity of warfarin INR

Disease
Coronary Artery Disease (CAD) Coronary Artery: sole purpose is to supply myocardial muscle. Coronaries come off the base of the aorta. Very rich in oxygen supply. Blockages lead to heart disease. Perfusion during diastole. Increased heart rate = decreased perfusion. Description: Also called atherosclerotic heart disease (ASHD). Affects 13.2 million in US; 500,000 deaths/year. Caused by atherosclerotic plague buildup in coronaries arteries. Results in obstruction to blood flow to myocardium.

Etiology/Risk Factors
Occurs over time CAD partial temporary obstruction (Angina) complete obstruction (MI) tissue death of heart Endothelium injury = increased atherosclerosis risk. Non-modifiable: age, gender, race, genetics Modifiable: smoking, obesity, inactivity, diet, oral contraceptives and hormone replacementbirth control pills especially problem for women who smoke. HyperlipidemiaLDLs promote cholesterol deposits on arterial walls. VLDLs: cary triglyceride HDLs: clear cholesterol from arteries, take back to liver for excretion; increase with exercise, weight loss, smoking cessation. hypertension, diabetes mellitus
1) Stable: Increased demand, decreased supply of oxygen. Rest-relieved. *Nitroglycerin. 2) Unstable Blood clot. Bleed. Blocked. Not related to activity (anytime can happen) *Morphine given 3) Prinzmetal: Vasospasms: *calcium channel blockers given-also for other forms of angina. Improves oxygen delivery to ischemic myocardium. Vasodilates coronary arteries, particularly used in treating prinzmetals angina. Reduces myocardial oxygen consumption. Decreases afterload. Non-dihydropyridines also lower heart rate and decrease contractility. Dihydropyridines may aggravate angina in some patients due to reflex tachycardia.

Assessment

Symptoms

Labs/Diagnostic Tests
Total serum cholesterol: increased levels = increased risk CHD. Pre draw instruction: Consistent intake of dietary cholesterol for 3 weeks. Fasting Lipid Profile: more specific than total serum cholesterol. Identifies levels of lipoproteins. Can calculate ratio between HDLs and total cholesterol (ideal 1:3). Triglygerides 40150 mg/dL (desire <150). NPO for 12 hours (after dinner).

Complications/Other Medications/Treatment Information

Diet: avoid high cholesterol. Low cholesterol (dietary cholesterol <200 mg/day) increase fiber (20-30 % fat; 50-60% CHO; 15% protein. Avoid transfats, these act like saturated fats. Include good sources of protein (nonfat dairy products; fish; poultry) increase monounsaturated fats (olives, canola, peanut oils); these decrease LDLs & increase HDLs. Smoking Cessation: rapidly decreases the risks. Those who stop decrease risks of CV disease by 50%. Lowers LDL, raises HDL Exercise: Must first be examined by health care provider. Recommend at least 30-45 minutes of moderate physical activity (aerobic). Lowers VLDL, LDL, triglycerides. 5-6 days per week. Control BP with low Na diet, increased Ca intake, regular exercise, stress management, medications. Control DM with diet, exercise and medications. Control hyperlipidemia with diet and medications

Angina (chest pain) Chest pain that results from temporary imbalance between myocardial oxygen supply & demand. Reduced blood flow leads to myocardial ischemia that is temporary and reversible. With ischemia cells shift to anaerobic metabolism. Lactic acid is produced; stimulates nerves; pain results. Necrosis results when blood to area is reduced for more than 30 minutes. Time is muscle

B-Adrenergic Blockers in the Treatment of Angina: Reduces myocardial oxygen consumption by reducing contractility and heart rate. Improves myocardial perfusion by slowing heart rate (more time spent in diastole). Prevent reflex tachycardia. Decrease mortality with MI. ACE inhibitors prevent cardiac remodeling. Decreases both preload and afterload. Decreases scarring.

Tight, squeezing, heavy pressure, or constricting sensation. Cresendodecresendo pattern usually lasting 2-5 minutes. Pain radiates to the jaw, neck, shoulders, left arm. Dyspnea, pallor, tachycardia, anxiety and fear. Women frequently present with atypical symptoms. Like indigestion

Watch for ECG changes. Echocardiogram: ultrasound to assess myocardial structure and functioning. Assess for mural thrombi. Transesophageal echocardiography (TEE) How much blood with contraction. NPO-check gag reflex. Ejection fraction-more sensitiveischemia caught well. Stress electrocardiography: uses ECG to monitor cardiac response during progressive exercise. No food or drink 2-3 hours prior to test. No beta blockers and caffeine. Assess for CI. recent MI, severe unstable angina, Dysrhythmias, CHF, and recent PE.

The major acute adverse effects of nitro vasodilators are due to excessive vasodilatation: orthostatic hypotension, tachycardiabeta blockers to decrease, severe throbbing headachedilation of brain, dizziness, flushing, syncope Slidenafil (Viagra), Vardenafil HCl (Levitra), Tanadafil (Cialis) can potentiate the actions of nitrovasodilators. Unsafe drop in BP. They should not be taken within 6 hours of taking Sildenafil.

Antianginal Drug: the drug of choice for treatment of an acute angina attack is Nitroglycerine taken by sublingual route-fast acting vasodilator. Sublingual Nitrates dilate coronary arteries. Take one dose. If that dose does not relieve pain, repeat it after 5 minutes. If after another 5 minutes the pain is still present, take a third dose. If after 5 minutes the pain is not relieved call 911. hepatic first pass NTG: rapid onset of action (1-3 min) when administered sublingually. Short duration of action (20-30 min) is not suitable for maintenance. Slowly absorbed preparations (oral, transdermal) provide prolonged prophylaxis against angina (3-10 hours) Can lead to tolerance. Nitrate free periods of at least 8 hours overnight. Tingly sensation = working!

Coronary Angiogram: Gold Standard for evaluating coronary vessels. Catheter introduced into femoral or brachial arteries. Catheter threaded retrograde coronary arteries. Dye injected. 50% occlusion = significant. 7075% occlusion = symptom. Cardiac Cath: similar to coronary angiogram; same initial procedure. Catheter may be threaded to coronary arteries for angioplasty (therapeutic). Catheter may be threaded to pulmonary artery for monitoring of cardiac pressures. Pre: no aspirin. informed consent must be signed. NPO 6-8 hours prior but can have fluids up to 4 hours prior. Routine cardiac drugs often given (check with MD). Check allergy to shellfish, iodine, iodine dye. Baseline check of pedal pulse; mark location. Teaching: client should know he/she will be awake but sedated. Should not feel pain. Ca have sense of metallic taste in mouth as dye is injected. Pulse may feel like it speeds up or skips beats. Lasts 1 or 2-3 hours. Post: vitals q 15 min for 1 hour; q 30 next hour; q 2-4 hours after. Bedrest 6-12 hr (artery seals). Pressure dressing on site; check bleeding. Liberal fluid to get rid of dye if no contraindications. CMS checks: check peripheral pulses of extremity, note color, warmth and cap refill, ask to wiggle toes, assess for ability to feel touch.

Disease
Myocardial Infarction=dead tissue. Heart attack Death of a portion of the heart muscle. CAD is the most common underlying cause of an MI. If myocardial ischemia last for 30 minutes

Etiology/Risk Factors

Assessment

Symptoms

Labs/Diagnostic Tests
White Blood Cells & ESR: inflammation, myoglobin increased in bloodstream. ECG changes **Understand Cardiac Serum Markers Chart!

Complications/Other Medications/ Information Treatment

Circulation: Percutaneous Transluminal Coronary Angioplasty with or without stent (PTCA). Or Percutanous Coronary Intervention (PCI) Nursing care similar to cardiac angiograpy CABG: surgical procedure that cracks open the chest and goes through leg. Goal is to reverse & prevent further damage on the myocardium. Time is muscle M= morphine; O= oxygen; N= nitro; A= aspirin Airway: maintain open airway Breathing: supplemental oxygen is needed to meet myocardial demand. Oxygen by nasal prongs (crank up) Circulation: sublingual nitroglycerin initially. Aspirin 160 to 325 mg. Start IV Nitro as per hospital protocol. Reduces ischemic pain by dilation of blood vessel, help in lowering BP, decreases venous return Thromolytic Therapy: within 3-12 hours: altepase, streptokinase, reteplase, anistreplase. Heparin drip post thrombolytic agent. Administer anti-arrhythmics if Dysrhythmias develop.

Collaborative Care: Monitor vital signs for changes and instability. Auscultate for lung sounds. 12 lead EKG. Continuous EKG monitoring for arrhythmia. Teach patient: cardiac diet, difference between MI and angina pain. When to take NTG. Take medications as directed. Smoking cessations. Stress reduction. Limit activities. Need for cardiac rehab (SEE HANDOUTS!! **). Lifestyle changes.

Disease
Peripheral Arterial Disease (PAD): when the arteries in their legs become narrowed or clogged with fatty deposits, or plague. The buildup of plague causes the arteries to harden and narrow, which is called atherosclerosis.

Etiology/Risk Factors

Assessment
(legs down) Acute pain Intermittent claudication Coldness Weak pulses Parasthesia Pallor when limb is elevated. Rubor when limb is dependent (down) Hair loss distant with occlusion Thick brittle nails No edema: but ulcers in distal areas, foot, toes, ankles and calves.

Symptoms
Intermittent claudication (stable angina of legs) Food or toe wounds that wont heal or heal very slowly. Gangrene (dry) A marked decrease in the temperature of your lower leg or foot Weak peripheral pulses

Labs/Diagnostic Tests
Doppler and Ultrasound (Duplex) Imaging: visualizes the artery with sound waves and measures the blood flow in an artery to indicate the presence of a blockage. Computed Tomographic Angiography (CT): a noninvasive test that can show the arteries in your abdomen, pelvis and legs. Magnetic Resonanace Angiography (MRA): a non-invasive test that gives information similar to that of a CT without using X-rays. Angiography: during this test a contrast agent is injected into the artery and X-rays are taken to show arteries in the legs and any blockages that may be present.

Complications/Other Information

Medications/Treatment
Stop smoking, avoid becoming chilled, wear warm socks, boots, gloves, warm water baths. Exercising to stimulate circulation-as long as it doesnt cause pain. Dont keep legs elevated. Antilipidemic Drugs. Anticoagulants & Antiplatelets, Vasodilators, Manage stress Peripheral Artery Angioplasty: for patients that conservative treatments arent enough. Peripheral Bypass Surgery: if theres a long portion of artery in your leg that s completely blocked and youre having severe symptoms, surgery may be necessary.

Thromboangiitis Obliterans (Buergers Disease) clot inflammation of vessel that blocks and kills tissue. Acute arterial occlusion. Inflammatory vasculitis causing the thrombus formation. Distal arterial ischemia. 2) Reynauds Disease Periodic constriction of arteries that supply extremities, mostly hands and feet.

1)

Non-modifiable: being a man, over 50, asian Modifiable: smoking (vasoconstriction, inflammation), obesity, hypertension, high cholesterol. Frequently seen in young women. Signs and symptoms usually precipitated by exposure to cold, emotional upset and tobacco usage.
Little or no pain, some tenderness along inflamed vein. Warm skin temperature Cyanotic if dependent position Edema typically present Pulses normal and

Pain: client learns warmth relieves pain. Relieves vasospasms, blood rushes to the extremity. Numbness Coldness Tingling lasts minuteshours.

Venous Disorders (Peripheral Venous Disease)

present

Thrombophlebitis/Venous Thrombosis (clot-inflammation) Formation of a thrombus in association with inflammation of vein. Classified as either superficial or deep. 65% of IV therapy-superficial 5% of surgical patients-deep -Clot-travels or emboli to lung

Superficial: palpable, firm, cordlike vein. Warm, redness, tenderness, edema, IV therapy-arms, varicose veins-legs. DVT: unilateral leg edema. Pain, warm skin, cyanosis possibly, positive Homans sign: pain upon dorsiflexion of foot. Not always present in all cases. Lungs make heparin, compartment syndrome. Virchows Triad: venous stasis/pooling , damage of endothelium of inner lining of vein. Hypercoagulabilty of blood. Moves slower. Specific risk factors: prolonged bed rest, obesity, varicose veins, hip/knee replacements, oral contraceptives Causes: atherosclerosis (primary reason) Hypertension (contributing factor) Location: Thoracic, abdominal, cerebral. Typically in the aorta.

Venogram: Non-invasive Doppler studies Coagulation studies: PT, PTT, INR, D-Dimer, FDP MRI Lung Scan if emboli (PE)

Prevention: Prophylaxis (Try to prevent from occurring especially high risk groups.) -Low molecular weight heparin for those at risk (surgery, bedrest) Early mobilization Leg exercise (ankle flexion and extension); helps venous flow by causing muscle compression on veins push blood flow from superficial veins into deeper veins-promote venous return to heart TEDS or pneumatic compression devices to legs.

Treatment: bed rest with leg elevated until tenderness is reduced. Dont massage legs, no SCD, no leg exercises. Anticoagulants like Heparin drip for acute treatment Warfarin, Plavix (Clipidrogel), Lovenox for prevention *Risk for bleeding Pain control: anti-inflammatory drugs. Warm moist heat (K-pad) may be used to relieve pain and inflammation. For chronic recurrent DVT: IVC filter.

Aneurysm Abnormal dilation of blood vessel. Commonly occurs at site of weakness or tear in vessel wall. Most often in aorta and some in peripheral arteries.

70 year old male Smoker High blood pressure CABG Cholecystectomy Inguinal Hernia Repair AAA

Ultrasound-most often used to diagnose AAA. MRI-determine precise measurement and size. Non contrast. CT Angiogram

Aneurysmectomy: open abdominal thoracic surgery , dissect out the aneurysm. Replace area with synthetic fabric graft, aneurysm walls generally sutured around graft. Endovascular Stent Graft (Endograft) Procedure: done for AAA (not thoracic), the stent (metal sheath covered with polyester fabric) is placed percutaneously with help of fluoroscopy to guide placement. Fabric tube that reinforces a weak spot in the aorta. Treatment: Endovascular Stent Graft (Endograft)

watchful waiting For aneurysm smaller than 5 cm, for patients with high BP, monitored every 6 months for changes in the aneurysm. Regular CT or Ultrasound. Manage medically. Pharmacology (esp if dissecting) Antihypertensives to lower BP in aorta -Nitride (Sodium Nitroprusside) IV to keep systolic pressure 120 mmHg or less in acute setting -Beta Blocker-Inderal IV over 5 minutes to decrease HR to 60/min After surgery and graft repair: Heparin IV for at least 1 week Then oral anticoagulants or ASA often for life to keep graft patent and free of clots

1)

Thoracic Aortic Aneurysm

Dyspnea, stridor, brassy cough (if pressing with laryngeal nerve) Deviation of trachea (if pressing on trachea) edema of head and face (if presses on SVC) distended neck veins (If presses on SVC), dysphagia (if presses on esophagus) depends on what parts its pressing on.

2)

Abdominal Aortic Aneurysm (more common) AAA

Usually occurs in those >70 90% occur below renal arteries.

Anatomy: depending on where the aneurysm forms: patient may have renal failure, decreased blood flow into lower extremity (s), decreased blood flow into gastrointestinal system. (deceased blood flow to GI and kidneys)

Most asymptomatic, pulsating mass in mid/upper abdomen, abdominal thrill, bruit over mass-turbulent blood flow, pain in mid abd or low back.

AAA Rupture:only 50% survive even with surgery (after rupture). Death from bleeding into peritoneal cavity. Manifestations: hypovolemic shock, lower extremity pulses absent Symptoms: sudden intense abdominal pain, pain radiating on back of legs, sweatiness/clamminess/dizziness, low BP, tachycardia, loss of consciousness

Primary sign: sudden Treatment excruciating pain (ripping Tear in the intima of the aorta, or tearing sensation) blood forced between layers of Abd aorta = aorta. Creates blood-filled cavity abdominal pain that can expand length of aorta. Thoracic aorta = chest or back pain Distal pulse absent as dissection further occludes blood flow. Paralysis eventually possible (decreased blood flow to spinal cord) Nursing Responsibilities: Pre-op: may do brief teaching if emergency. Deal with clients fear and anxiety. Watch signs of impeding rupture and expansion. Decrease risk of rupture. Watch for emboli. Pain control. Administer anti-hypertensive meds. Post: teaching, no heavy lifting, strenuous exercise, sex (6-12 weeks), no prolonged sitting, avoid constipation, no smoking, must warn MD and dentists for rest of life when about to have procedures, since graft in place will need prophylactic antibiotics (bacteria grow on grafts) (organisms migrate to graft sites). Also anticoagulants for life. Follow up CT.

3)

Aortic Dissection

Hypertension Hypertension defined as: Systolic BP of ____________ mmHg or > OR Diastolic BP of _________ mmHG or > on the average of 3 or more readings taken on separate occasions Age of onset 25 55 Greatest occurrence in African Americans Major public health issue Rarely causes symptoms BUT major risk factor for CHD, heart failure, stroke, renal failure Etiology of Hypertension Primary HTN 90-95% of cases Also termed essential of idiopathic NO known cause but risk factors include: Family history Increased Na Intake Obesity Inactivity Excessive Alcohol intake Secondary HTN About 5% of cases Renal or renovascular disease Endocrine disease Pheochomocytoma Cusings syndrome Conns syndrome Primary HTN Risk Factors Non-modifiable Family History Age > 50% in ages 60 69 75% in ages 75 and older Race Nearly 40% of African American adults are hypertensive Insulin resistance Modifiable Diet High Na Intake Obesity Excess alcohol consumption Alcohol causes vasoconstriction Stress High level of catecholamines Smoking Causes vasoconstriction Complications of Diabetes Myocardial Infarction & heart failure Renal Failure

Stroke Retinopathy Assessment: Subjective Family history of HTN or CVD Reports of fatigue, blurred vision, & headache Reports of dyspnea on exertion, palpitations, angina, weight gain, edema Objective Elevated BP Peripheral edema, retinal vessel damage, diminished or absent peripheral pulses, bruits, murmur, and S3 and S4 hear sound Diagnostic Tests: Elevated cholesterol & triglyceride Elevated BUN & Createnine Abnormal Urinalysis Cardiomegaly on CXR Abnormal ECG Nursing Diagnosis Decreased cardiac output Ineffective Health Maintenance Risk for non-compliance Planning and Implementation Inform client that hypertension is usually asymptomatic Tell client to keep record of BP readings Explain the need for long term therapy and follow-up Client education: Sodium restriction Weight reduction For every kg of lost weight there is a 1.6/1.1 mm Hg loss in systolic and diastolic blood pressure Aerobic exercises 30 45 min per day, 5 6 days a week. Dietary Approaches to Stop Hypertension (DASH) Includes prescribed number of servings of food in the following categories Grains 7 8 servings/day Vegetables 4 5 servings/day Fruits 4 5 servings/day Nonfat/Low-fat diary products 2 3 servings/day Mean, poultry, & fish 2 or less 3oz serving/day Nuts, seeds, & dry beans 4 5 servings/week Fats & oils 2 3 servings/day Sweets 5 serving/week (low fats) Rich in fruits, vegetables, and low-fat dairy products Reduce cholesterol, saturated, and total fat Increased K, Mg, protein and calcium Planning and Implementation Alcohol Consumption Recommended alcohol intake for hypertensive: No more than 1 oz ethanol or 2 drinks per day

A drink is 12 oz of beer, 5 oz of wine, or 1.5 oz of 80-proof whiskey Women and lighter weight should reduce this limit by half Planning and Implementation

Smoking Cessation Nicotine is a vasoconstrictor. Definitive link exist between smoking and heart disease. Reduces efficacy of beta-blockers Nicotine patches and gums contain lower amount of nicotine and usually do not raise BP Medications Diuretics- prompt kidneys to excrete sodium, which reduces blood volume and thus blood pressure Adrenergic Blockers: Beta blockers - Slows heart beat and lessens force of hearts contractions by blocking B1 receptors Alpha blockers Promotes vasodilation by blocking alpha1 receptors on arterioles. Centrally acting adrenergic agonist Act with in the CNS to stimulate alpha2 receptors causing a decrease release of norepinephrine and resultant reduction in sympathetic outflow Calcium Channel Blockers - prevents calcium from enabling muscles cells to constrict around the blood vessels, thus dilating the vessels ACE inhibitors - Dilates blood vessels by blocking enzymes which cause artery walls to constrict DIURETICS Drugs that can Decrease Preload Purpose is to block absorption of Na & Cl in the kidneys, thereby decreasing the volume of water reabsorption. Decrease the plasma and extracellular fluid volumes Results: Overall effect: Loop Diuretics: Furosemide (Lasix) Bumetanide (Bumex) Most potent diuretic Thiazide Diuretics: Hydrochlorothiazide (Hydrodiuril) Chlorothiazide (Diuril) Chlorthalidone (Hygroton) Metolazone (Zaroxolyn) Indapamide (Lozol) Osmotic Diuretics: Mannitol (IV drip) Potassium Sparing Diuretics: Amiloride (Midamor) Triamterene (Dyrenium) Spironolactone (Aldactone) Eplerenone (Inspra) Decreased workload of the heart Decreased blood pressure Decreased preload Decreased cardiac output

Non-Potassium Sparing Diuretics Can cause Hypokalemia Loop Diuretics Thiazides Potassium Sparing Diuretics Can cause Hyperkalemia Blocks aldosterone receptors Spirinolactone (Aldactone) Eplerenone (Inspra) Nursing Responsibilities Monitor for electrolyte imbalance: K level Cardiac dysrthytmias Muscle weakness Daily weight: Report weight gain of more than 2 3 lbs Teach how to prevent orthostatic hypotension Avoid foods high in K if taking potassium sparing diuretics (Banana, Oranges, Apricot, Tomato Juice, Salt substitute) Take potassium supplement as ordered if on non-potassium sparing diuretics May potentially increase blood level of other toxic drugs Alpha1-Receptor Antagonists Doxazosin (Cardura) Prazosin (Minipress) Terazosin (Hytrin) Blocks alpha1-receptor on arterioles causing vasodilation Side Effects Dry mouth, Drowsiness, Sedation, Constipation, Reflex Tachycardia, Nasal congestion, Incontinence, Impotence HIGH INCIDENCE OF ORTHOSTATIC HYPOTENSION first Dose effect 30 60 min after first dose Give at hs or initial dose should be 1/3 or of the normal dose Teach prevention of orthostatis and monitor BP regularly Adrenergic Blocking Agents

Beta-blockers Act in the periphery by blocking beta receptors 2 types: Cardioselective primarily affecting 1 Non-cardioselective affecting both 1 & 2 Reduce heart rate due to beta1-blockade Bronchoconstriction due to Beta2-blockade All the names of -blockers ends in lol Examples: Propranolol (Inderal), Atenolol (Tenormin). Metropolol (Lopressor), Nadolol (Corgard) Adrenergic Blocking Agents Side effects Impotence Bradycardia Fatigue

Mask symptoms of hypoglycemia Bronchoconstriction CI to asthmatic patients Arrhythmia if stopped abruptly due to upregulation of receptors Taper of gradually for 1 week Nursing Responsibilities Monitor VS and compare to baseline Check HR before giving the drug, hold and inform MD if HR is < 60bpm Teach prevention of orthostasis Avoid Beta blockers in clients with COPD & Asthma Caution in use of beta blockers with diabetic patients Centrally Acting Adrenergic Agonist Clonidine Methydopa Act within the CNS to stimulate alpha2 receptors Decrease release of norepinephrine Reduction in sympathetic outflow to blood vessels Venous and arterial dilation Examples: Clonidine (Catapress) Methyldopa (Aldomet) Adverse Effects Dry mouth Sedation Impotence Constipation Rebound hypertension when stopped abruptly Depression Nursing Implications Teach client: Use sugarless gum or hard candy for dry mouth Prevent alcohol Report signs of depression Consult MD before stopping medication Inform MD if you are taking some antidepressant drugs DRUGS AFFECTING THE RAAS Angiotensin-converting enzyme inhibitors Angiotensin II receptor blockers Decreases Both preload & Afterload Renin-Angiotensin-Aldosterone System Actions of angiotensin II Vasoconstriction Release of aldosterone ACE Inhibitors: Captopril (Capoten) Enalapril (Vasotec)

Lisinopril (Prinivil and Zestril) Quinapril (Accupril) Ramipril (Altace) Angiotensin Converting Enzyme (ACE) Inhibitors ACE inhibitor prevents angiotensin I from converting into angiotensin II Reduce vascular resistance by promoting vasodilation Decrease blood volume by stopping release of aldosterone Renal protective effects in patients with diabetes Drugs of choice in hypertensive patients with DM ACE Inhibitors: Side Effects Fatigue Dizziness Headache Fetal Injury Hyperkalemia Renal failure Monitor BUN & Createnin Neutropenia Monitor WBC Dry, nonproductive cough, which reverses when therapy is stopped (Due to Bradykinins) Angioedema (Bradykinins) NOTE: First-dose hypotensive effect may occur! Nursing Responsibilities Monitor VS and compare with baseline Monitor potassium level Know BUN and Createnine before beginning treatment Hold and inform MD if BUN and Createnine increases Teach prevention of orthostasis Not for pregnant women Aspirin and NSAID can decrease the efficacy of ACE inhibitors Teach patient that Dry cough is common adverse effect Monitor for swelling in face and throat during initiation of treatment Angiotensin II Receptor Blockers (ARB) Mechanism of Action: Allow angiotensin I to be converted to angiotensin II Block the receptors that receive angiotensin II Block vasoconstriction and release of aldosterone Advantage: Do not cause a dry cough Examples: Losartan (Cozaar, Hyzaar) Valsartan (Diovan) Olmesartan (Benicar) Irbesartan (Avapro)

Angiotensin II Receptor Blockers: Side Effects Headache May cause occasional dizziness, inability to sleep, diarrhea, dyspnea, heartburn, nasal congestion, back pain, fatigue Hyperkalemia Fetal harm Renal failure Nursing Responsibilities Monitor VS and compare with baseline Monitor potassium level Know BUN and Createnine before beginning treatment Hold and inform MD if BUN and Createnine increases Teach prevention of orthostasis Maybe taken with or without meal Not for pregnant women Aspirin and NSAID can decrease the efficacy of ARBs Fluconazole may increase antihypertensive effects Rifampin may decrease antihypertensive effect CALCIUM CHANNEL BLOCKERS Decreases Afterload Mechanism of action: Prevent calcium ions from entering cells Greatest effects on the heart and blood vessels 2 types: Dihydropyridines (affects blood vessels) Non-Dihydropyridines (affects both blood vessels & Heart) Dihydropyridines (Affects blood vessels) Amlodipine (Norvasc) Filodepine (Plendil) Nicardipine (Cardene) Nifedipine (Procardia) Agents ONLY act on Vascular Smooth Muscle This causes decreased peripheral smooth muscle tone and decreased systemic vascular resistance (vasodilation) Result: decreased blood pressure Adverse Effects Hypotension Flushing Constipation Dizziness Headache Reflex tachycardia (Rapid acting) Nursing Responsibilities Monitor VS and compare to baseline Teach prevention of orthostasis Assess for reflex tachycardia Stool softener and ambulation to prevent constipation

Non-dihydropyridines Acts BOTH on heart and blood vessels Diltiazem (Cardizem, Dilacor) Verapamil (Calan, Isoptin) Hemodynamic effects Vasodilation Decrease heart rate Decrease contractility Verapamil and Diltiazem: Side Effects Cardiovascular Hypotension Bradycardia Heart block Gastrointestinal Constipation Nausea Monitor VS and compare to baseline Check HR before giving the drug, hold and inform MD if HR is < 60bpm Teach prevention of orthostasis Stool softener and ambulation to prevent constipation Monitor ECG VASODILATORS Mechanism of Action Directly relax arteriolar smooth muscle Result: decreased systemic vascular resistance (decreased afterload) Drugs Under this Class: Diazoxide (Hyperstat) Hydralazine HCl (Apresoline) Sodium nitroprusside (Nipride, Nitropress) Nitroglycerine (Tridil) Adverse effects related to vasodilation Postural hypotension Reflex tachycardia Nursing Implications Hydralazine (Apresoline) Administer IM or IV in hypertensive crisis Take oral medication with food Monitor daily weight Can cause SLE like symptoms Na Nitriprusside (Nipride) Protect from light, heat & moisture Cover IV bag and tubing with foil Discard any solution that is not light brown in color

Administer with sodium thiosulfate to reduce risk of cyanide toxicity

Nitroglycerine (Tridil) IV infusion only Use only glass bottle and administration set provided Gradual wean off IV dose -pril------------------------------- ACE Inhibitor -lol or olol ------------------Beta Blocker -pine --------------------- Ca Channel Blocker -zosin --------------- alpha blockers -nitr ------------- nitrates Alpha Blockers Beta Blockers Ca Channel Blockers ACE Inhibitors Nitrates -lol -pril -pine -nitr -zosin Drugs for Heart Failure Causes Chronic hypertension Myocardial infarction Valvular heart disease Coronary artery disease Congenital heart disease Dysrhythmias Aging of the myocardium HEART FAILURE WHAT IS IT? Decreased Cardiac Output Heart failure is a condition where the heart cannot pump enough blood throughout the body. It means that your heart is not able to pump blood the way that it should. The heart cannot fill with enough blood or pump with enough force or both. A clinical syndrome comprising of dyspnea, fatigue or fluid retention due to cardiac dysfunction, either at rest or on exertion, with accompanying neurohormonal activation.

Clinical Manifestations Right sided failure Jugular venous distention Hepatomegaly Peripheral edema Sacral edema Left sided failure

Pink Frothy Sputum Dyspnea Cyanosis SOB Crackles at base of lungs Orthopnea Fatigue PND Compensatory Mechanisms With failure there is drop in CO Entire body receives less blood Body thinks Blood Volume has dropped Compensatory mechanisms begin: SNS Stimulation RAAS Cardiac Remodeling Release of ANP & BNP Heart Failure Compensatory Mechanisms Sympathetic N.S. stimulation Low CO affects SNS Baroreceptors sense drop in blood volume Stimulate sympathetic system to release epinephrine & norepinephrine Results in: Increased HR & contractility Vasoconstriction Initial increase in CO Renin-Angiotensin-Aldosterone Activation Low CO means drop in blood to Kidneys Kidneys then secrete ________ Renin causes Angiotensin I to change to II (vasoconstriction) Also release of aldosterone (retention of Na & water) Ventricular Remodeling Ventricular hypertrophy and dilation Ventricular chambers enlarge to accommodate increased fluid volume Initially increases force of contraction increases Remember Frank-Starling Law??? All mechanisms over long-term cause deterioration of cardiac function Mechanisms work for only for sometime Eventually cause more harm than good Mechanisms lead to fluid retention (congestion) Over stretching of the heart leads to poor contractility Frank-Starling Law

Acute Heart Failure Key Investigations 12 lead ECG, Chest X-Ray, Blood gases U&Es Electrolyte imbalance BNP Amino acid peptide, can be measured easily in blood Elevated in heart failure, therefore low BNP effectively excludes heart failure Echocardiogram Monitor for Possible Complications & Risk factors: Liver Function BUN & Createnine Modern treatment of chronic heart failure The present - neurohormonal hypothesis Drugs that inhibit the renin-angiotensin-aldosterone system (RAAS) ACE Inhibitors Can decrease both preload and afterload Prevent cardiac remodeling Diuretics Diuretics decrease plasma volume (preload). Relieve pulmonary congestion and peripheral edema. Loop diuretics are used for patients who require extensive diuresis Modern treatment of chronic heart failure The present - neurohormonal hypothesis Beta-Blockers Inhibit sympathetic nervous system activity on the heart Decrease the force of myocardial contraction & slow HR THEREFORE LARGE DOSES AVOIDED Aldosterone receptor blockers Example of this drug? Decreases preload How? Modern treatment of chronic heart failure The present - neurohormonal hypothesis Digoxin [Lanoxin, Lanoxicaps, Digitek] Increase strength of myocardial contraction by increasing intracellular calcium concentration Slow heart rate Positive Inotropic and negative chronotropic ALWAYS check AP before giving; hold and notify MD if < 60/min Narrow therapeutic range (0.5-2 ng/ml) Signs of toxicity A, N, V, HA, yellow vision, confusion Watch K levels; if low = increased risk toxicity

Vasodilators Arterial dilators reduce SVR (decrease afterload) Venous dilation decreases venous return (decrease preload) Nitrates (Tridil) Na Nitroprusside (Nipride) Calcium-channel blockers should be avoided in patients with HF Decompensatory Stage Cardiogenic Shock Patient is manifesting signs of poor perfusion Treatment includes inotropes Dobutamine Dopamine Patient will require hemodynamic monitoring Nursing Interventions Decreased Cardiac Output Monitor vital signs Check breath sounds (crackles in lungs with SOB condition worse) Assess for signs of decreasing C.O. (these show signs decreased tissue perfusion to other organs) Change in LOC (confusion) Drop in urine Cool, clammy skin (blood shunted from periphery) Diminished pulses Supplemental O2 as ordered Rest; HOB elevated to decrease work of breathing; Bedside commode; no Valsalva since increases heart workload Quiet environment (decrease O2 consumption) Nursing Interventions Fluid Volume Excess - Compensatory mechanisms cause salt and water retention Assess resp (declining resp status, indicator of worsening left heart failure Notify MD immediately if: Air hunger Sense of doom Tachypnea Orthopnea Pink frothy sputum (acute pulmonary edema is medical emergency) Careful I & O (notify MD if output < 30cc/hr) Weigh daily (1 L of fluid = 2.2lbs weight) Measure abd girth q shift (same time; same place on abd) Bedrest with HOB elevated 45 degrees (decreases venous return to heart and decreases work on heart) Restrict fluids as ordered

Medications: Test 3

Fractures: Narcotics, NSAIDs, Stool Softener Osteoporosis:

Estrogen replacement therapy (ERT) Used to prevent and treat osteoporosis For surgical menopause before age 50 Decreases osteoclastic activity & increases osteoblastic activity Can increase risk of endometrial cancer. Advantages: increases bone density, decreases risk of fractures, relief of hot flashes, vaginal dryness, decreases LDL, increases HDL Disadvantages: increased risk of urterine ca (if unopposed), increased risk of DVT, possible increased risk of breast and endometrial cancer Dose: Estrogen- 0.625 mg, qd, 0.3 mg; Progesterone- 2.5 mg, qd, (if uterus is present) Selective estrogen receptor modulators (SERM) Treatment and prevention of osteoporosis by mimicking estrogen beneficial effects on bone density. Decreases bone resorption Advantages: increases bone density, decreases fracture risk, no stimulation of breast or endometrial tissue, decreases LDL Disadvantages: increased risk of DVT-not for women with history of blood clots, doesnt treat post menopausal symptoms-may increase hot flashes, no effect on HDLs Dose: Raloxifene (Evista) 60 mg, qd Bisphosphonates Alendronate (Fosamax) 5-70 mg once a week dosing Risendronate (Actonel) 5-30 mg once a week dosing Ibandronate (Boniva) 150 mg once a month Primidronate (Aredia) & Zoledronic (IV prep) Prevention & treatment of osteoporosis in post menopausal women. Prevention and treatment of steroid-induced osteoporosis both in men & women, Pagets disease, hypercalcemia of malignancy It absorbs to hydroxypatite and becomes a part of the bone structure. Bisphosphonates prevent bone resorption by inhibiting osteoclast activity. Take on empty stomach. Take first thing in the morning (30 min before meal). No food or other meds 30 minutes after taking Bisphosphonates. Take with 8 oz of water only. Remain in an upright position for at least 30 minutes after taking the drug-result in esophagitis and GI distress. Instruct patient to report chest pain or dysphagia. Separate Ca, Al, and Mg containing meds by at least 4 hours. Advantages: increases BMD, decreases fracture risk, no increased risk of breast and uterine ca or thromboembolic events, weekly or monthly dosing. Disadvantages: risk of GI disorders, contraindicated in renal failure Calcitonin Increase in blood calcium increases secretion of calcitonin decrease in blood calcium increases secretion of parathyroid hormone Principal effects are to lower serum calcium and phosphate Salmon calcitonin (Miacalcin, Calcimar) Nasal spray o It inhibits osteoclast activity, decreases bone resorption thus lowers serum calcium and phosphate and reduces bone pain, it increases BMD in the spine. Pagets disease, osteoporosis, hypercalcemia. o Side effects: sore, itching, rhinitis. Transient ANV, urinary frequency, flushing of face, palms and soles of feet. Risk of anaphylaxis. Take adequate amount of calcium and vitamin D. take in evening. Warm to room temperature, use alternate nostril. ANV may occur. Report nose bleeds.

Arthritis:
Osteo: Acetaminophen, NSAIDs, Glucocorticoids-maybe injected directly into the joint directly (not more than every 4-6 months) Rheumatoid: Acetaminophen, NSAIDs, glucocorticoids Disease Modifying Anti-Rheumatic Drugs (DMARD) Gold salts, hydroxychloroquine (Plaquenil)-base line eye exam every 6 months, Sulfasalazine (Azulfidine) & Dpenicillamine (Cuprimine) Immunosuppressant agents Imuran, Cytoxan, Rheumatrex Biologic immunosuppressant Gouty: Chemotherapy, thiazide diuretics, aspirin, TB drugs, NSAIDs, corticosteroids, cholchicine, allopurinol Colchicine: Anti-inflammatory effects limited to gout. Inhibits crystal-induced production of chemotactic factors Side effects: PO-abdominal cramping, diarrhea, nausea, vomiting. IV- local pain, DIC, tissue damage on extravasation. Contraindicated- GI, renal, hepatic, or cardiac disease Urate lowering drugs Goal is for serum urate concentrated to be <8 mg/dL Xanthine oxidase inhibitors-blocks conversion to uric acid o Allopurinol Uricosuric drugs- inhibits tubular absorption o Probenecid or Sulfinpyrazone

Knee & Hip Replacements: pre-antibiotics, enoxaparin (lovenox), fondaparinux (arixtra), Coumadin (Warfarin) Alzheimers Disease:
Acetylcholinesterase Inhibitors: selectively inhibits acetylcholinesterase which enzymatically degrades acetylcholine which is needed to be a neurotransmitter dealing with learning and memory. Tacrine (Cognex)-one hour before meals (hepatoxic); Donepezil (Aricept)-at bed time; Rivastigmine (Exelon); Galantamine (Razadyne)-with food, substrate of p450 Adverse effects: Cholinergic related problems: urinary retention, seizure, bradycardia, GI bleeding. NMDA-receptor Antagonists - blocks the activation of glutamate receptors and minimizes the adverse effects of excess glutamate Metamantine has shown to slow rate of memory loss in both vascular-associated and Alzheimers dementia. Well tolerated. Side effects: confusion, agitation, restlessness, indistinguishable from AD symptoms

CVA:
Thrombolytics and/or heparin-not for hemorrhagic TPA: 3 hours of onset of symptoms to dissolve the clot Edema: mannitol, loop diuretics Seizures; dilantin, valium, ativan, Phenobarbitals

Increased ICP:
Stress ulcers: H2 blockers, Esomeprozole Furosemide & Mannitol- draw water from edematous tissues into vascular space, Phenytoin Glucocorticoids help relieve cerebral edema

Epilepsy:
Anti-Epileptic Drugs (AEDs) Modification of ion conductances. Decrease in Sodium, Calcium influx (delay depolarization/prolong repolarization) Increased Chloride influx (hyperpolarizes membranes) Increase inhibitory (GABAergic) transmission Increased Chloride influx (hyperpolarize membrane) Decrease excitatory (glutamatergic) activity

Decrease sodium, calcium influx (delay depolarization/prolong repolarization)

Many CNS drugs act on GABA receptors to effect the frequency and duration of action potentials! Choosing Antiepileptic Drugs: Monotherapy for Partial Seizures: Best evidence and FDA indication: Carbamazepine (Tegretol), Oxcarbazepine, Phenytoin (Dilantin), Topiramate (Topamax) Similar efficacy, likely better tolerated: Lamotrigine (Lamictal), Cabapentin (Neurontin), Levetiracetam (Keppra) As shown to be effective: Valproate (Depakote), Phenobarbital, Felbamate, Lacosamide Limited data but commonly used; Zonisamide, Pregabalin Monotherapy for Generalized-Onset Tonic/Clonic Seizures Best evidence & FDA indication: Valproate, Topiramate Also shown to be effective: Zonisamide, Levetiracetam (Keppra) Phenytoin (Dilantin), Carbamazepine (may exacerbate absence and myoclonic sz) Lamotrigine (may exacerbate myoclonic sz of symptomatic generalized epilepsies) Absence seizures Best evidence: Ethosuximide (limited spectrum, absence only) Valproate (Depakote) Also shown to be effective: Lamotrigine (Lamictal) May be considered as second-line: Zonisamide, Levetiracetam, Topiramate, Felbamate, Clonazepam Myoclonic Seizures Best evidence: Valproate (Depakote) Levetiracetam (Keppra) (FDA indication as adjunctive tx) Clonazepam (Klonopin) (FDA indication as adjunctive tx) Possibly effective: Zonisamide, Topiramate (Topamax) Common Side Effects of AEDs: Often dose related: dizziness, fatigue, ataxia, diplopia, irritability-Keppra, word-finding difficulty-Topamax Weight loss/anorexia: topiramate, zonisamide, felbamate Weight gain: valproate (also associated with polycystic ovarian syndrome in young women) Carbamazepine, gabapentin, pregabalin Serious Side Effects: Typically idiosyncratic: renal stones (topiramate, zonisamide); hyponatremia (carbamazepine, oxcarbazepine), aplastic anemia (felbamate, zonisamide, valproate, carbamazepine); agranulocytosis (Carabamazepine (Tegretol)); hepatic failure (valproate, felbamate, lamotrigine, phenobarbital); Anhydrosis, heat stroke (topiramate); Acute closed-angle glaucoma (topiramate) Phenytoin Adverse Effects: Acute toxicity: high IV rate: cardiac arrhythmias + or hypotension &CNS depression. Acute oral overdose: cerebellar and vestibular symptoms and signs: nystagmus, ataxia, diplopia vertigo Chronic toxicity: dose related vestibular/cerebellar effects, behavioral changes, gingival hyperplasia, GI disturbances, Sexual endocrine effects, osteoporosis, hirsutism, hyperglycemia Drug Interactions: Sulfonamides, valproate and phenylbutazone: displace phenytoin from binding sites Cimetidine, disulfiram, doxycycline, isoniazid, phenylbutazone, sulfas, Warfarin, chloramphenicol: inhibits phenytoin metabolism -

Barbiturates & carbamazepine, pyridoxine, theophylline, alcohol: enhance phenytoin metabolism Phenytoin decreases serum levels of: carbamazepine, chloramphenicol, corticosteroids, haloperidol, quinidine, theophylline, oral contraceptives, Warfarin

Valproates: Precautions & Contraindications: Pregnancy category D associated with spina bifida. Uncommon but may impair platelet aggregation (bleeding time maybe prolonged). Can cause bone marrow suppression (Baseline CBC & regular monitoring). Can cause false positive ketone urine test in diabetic patients. Heptotoxicity and liver failure-Do not take with alcohol! Carbamazepine Drug Interactions: Increase carbamazepine levels via decreased metabolism: cimetidine, erythromycin, isoniazid Decrease carbamazepine levels via increase metabolism: phenytoin, valproic acid Carbamazepine decreases drug levels: Warfarin, oral contraceptives, doxycycline, phenytoin, haloperidol Carbamazepine increases drug levels: cimetidine, isoniazid Lithium induces carbamazepine toxicity Phenobarbital Drug Interactions: Increase Phenobarbital levels, acute ethanol ingestion, chloramphenicol, valproic acid Decreases Phenobarbital levels via increased metabolism, chronic alcohol ingestion, pyridoxine, rifampin Barbiturates decrease serum levels: tricyclics, Warfarin, beta blockers, oral contraceptives, digoxin, doxycycline, metronidazole, theophylline

Multiple Sclerosis
Immunomodulators 4 drugs currently available. Recommended for all patients with relapsing-remitting MS and with secondary progressive MS experiencing acute exacerbations. Self injected. Inferferon Beta 1a (Avonex and Rebif): is a protein that is a replica of human interferon. It suppresses the immune system and helps to maintain the blood-brain barrier. You inject Avonex into the muscle once a week and Rebif is injected under the skin 3 times a week. This drug is useful to people who have definite progressive MS. (T cells cant get back in, suppresses antiinflammatory cytokine. Cytokines communicate between WBCs). Interferon Beta 1b (Betaseron): is slightly different from our own interferon. This medication does the same thing as beta 1a, but is injected just under the skin every 2 days. This is also given to people who have definite progressive MS. Adverse Effects of Interferon: Flu-like reaction, hepatotoxicity, myelosuppression, injection-site reactions, depression

Glatiramer Acetate (Copaxone): is a small fragment of a protein that resembles a protein in myelin. Protects myelin by inhibiting immune response to myelin basic protein (competitive binding to APC). It decreases the reoccurrence of relapse. It is injected just under the skin every day-patient teaching! There is no flu like symptoms but occasional redness may occur at the injection site. A few amount of people do experience brief shortness of breath.

Immunosuppressants: Only 1 approved by the FDA-Mitoxantrone (Novatrone) More toxic than immunomodulators. Produces greater suppression of immune function: myleosuppression, hepatotoxicity, cardiotoxicity, fetal harm, Pancytopenia (risk for bleeding, infection & anemia) Monitor: perform CBC at baseline and prior to each dose. Perform LFT at baseline and prior to each dose. Perform pregnancy st test prior to each dose. Determine LVEF: prior to 1 dose, prior to all doses once the cumulative dose has been reached. Whenever signs of CHF develop (signs at 30% of ejection function; normal at 60-70%) Imuran; Cytoxan: suppresses immune system. Watch for bone marrow suppression (Pancytopenia-infections, fatigue/anemia, bleeding)

Supportive Drugs for MS: Spasticity-Baclofen, Tizanidine, Diazepam (Valium), Dantrolene Optic Neuritis-Methylprednisolone, Oral steroids Fatigue-antidepressant, amantadine Pain-Codeine, Aspirin Sexual dysfunction-Viagra Tremor-Primidone, Propanolol

Parkinsons Disease
2 major categories: Dopaminergic agents a. By far the most commonly used for PD. Promotes activation of dopamine receptors b. Levodopa (Dopar) & Lepodopa/Carbidopa (Sinemet) Dopamine + Carbidopa (Sinemet): Dopamine (DA) cannot cross BBB. Given as its precursor, levodopa or L-dopa, which is converted to DA by dopa-decarboxylase. Levodopa (L-dopa)-can cross BBB! Dopamine (DA) by dopa-decarboxylase Carbidopa inhibits peripheral decarboxyalse which is an enzyme that breaks down L-dopa. Thus, lower doses with fewer systemic side effects have the same beneficial CNS effects. Drug of choice (most effective agent to date). Most effective for bradykinesia, poor for tremor. Side Effects: o Wearing off effect-effectiveness wanes after 2-5 years. Initially, L-dopa effects last 6 hours after PO dose. Reduces to 3 hours after 2 years. Only 2 hours after 5 years of use. Remedy: drug holiday taper off over 3-4 days. o On-off phenomenon-fluctuating response to medication. Patient typically worsens suddenly for half hour then improves. Remedy: decrease dose and increase frequency. Sustained release Sinemet-CR may help. Bromocriptine, pergolide and selegiline may help. Palidotomy may help (surgery). o N/V common, psychiatric disturbances: hallucinations, confusion, nightmares are common. Tardive Dyskinesia (Michael J Fox)-orofacial in elderly, lip smacking, eye rolling, limb chorea/dystonia in younger patients. Overdose-GI upset, choreic movements. Can cause increase in IOP-contraindicated for glaucoma patients, can cause cardiac Dysrhythmias, hypertension Interaction of Sinemet: Pyridoxine (B6)-increases peripheral breakdown of levodopa. Concomitant administration with Mono Amine Oxidase Inhibitor (MAOI)-antidepressant Can lead to hypertensive crisis. Levodopa: promotes dopamine synthesis Dopamine agonists: stimulate dopamine receptors directly. Used for patients requiring larger doses of levodopa. Those experiencing motor fluctuations. Ergot Derivatives: Bromocriptine (Parlodel): stimulates primarily D2 DA post synaptic receptors. Acts as weak D1 antagonist. Causes Vasospasm!Contraindicated in patient with PVD/CAD!!* Pergolide (Permax): more potent than bromocriptine. Directly stimulates both D1 & D2 receptors. May reduce on-off phenomenon. Hypertensive patients shouldnt take this. Non-Ergot Derivatives: Bind selectively to dopamine D2-like receptors and activate D3 receptors which have unknown function. Parmipexole (Mirapex): has activity at D2 & D3 receptors Ropinirole (Requip): Strong D2 receptor agonist. Does not cause vasospasm. For patient with PVD. Selegiline (Eldepryl) & Rasagiline: inhibits dopamine breakdown in the brain by inhibiting MAO type B. Selegiline metabolized into amphetamine Amantadine (Apokyn): promotes dopamine release. These drugs stimulate the actions of dopamine in the brain, reducing the symptoms of Parkinsons disease (PD). 0.2-0.6 mL sub-Q prn maximum 5 times per day. Rescue med for acute, intermittent hypomobility, and off episodes (end of dose wearing off and unpredictable on/off episodes). Significant improvement in mobility at 20 minutes. Half life 40 minutes. Pregnancy category C. RESCUE MED. 1)

Cross sensitivity with Zofran. Severe N/V-start Tigan 3 days prior to initiation of therapy. Hallucinations, sudden sleep episodes, syncope, MI, Cardiac arrest, Priapism, Abuse potential COMT inhibitors: enhances effects of levodopa by blocking its degredation Methylation of Levodopa by this enzyme is a minor pathway of levodopa metabolism. This enzyme increases to compensate for a decrease in Dopa-decarboxylase with Carbidopa. Blocking COMT will increase peripheral blood level of levodopa and greater concentration of brain dopamine. Entacapone & Tolcapone 2) Anticholinergic agents a. Prevents activation of cholinergic receptors. Blockage of cholinergic transmission produces effects similar to augmenting dopaminergic transmission (balances dopamine/Ach ratio). b. Benztropine (Cogentin)

Myasthenia Gravis (MG)

Anticholinesterase Test: Edrophonium (Tensilon)- Rapid onset of 30 seconds. Short duration 5 minutes. Draw up 10 mg, Administer 2 mg. Monitro for adverse symptoms. Administer remaining 8 mg. Improvement of weak muscles that last 5-10 minutes. Test positive. Anticholinesterase Drugs: first line treatment for symptoms of MG. Do not treat the underlying disease. Pyridostigmine (Mestinon) no standard dose. Neostigmine (Prostigmin)- seldom use. *Atropine antidote for cholinesterase (ChE) inhibitor drugs. Must be available. Pyridostigmine (Mestinon): last 3 to 6 hours. Goal to produce maximal muscle strength with minimal side effects. Muscarinic Receptors- cholinergic (parasympathetic acetylcholine) receptors come in variety of types. One type is muscarinic receptors or mAChRs. Main end receptor stimulated by acetylcholine released from postganglionic fibers in the parasympathetic nervous system. Stimulation of muscarinic receptors causes parasympathetic ANS responses. Side effects: GI: heartburn, belching, abd cramps, increased peristalsis, diarrhea, N&V. GU: involuntary micturiction, increased tone and motility of uterus. CV: bradycardia, Vision: blurred, constricted pupils. Pulm: bronchoconstriction/bronchospasm, increased bronchial secretions, wheezing cough. Other: profuse sweating, increased salivation. Immunosupapression: For those who do not respond to anticholinesterase drugs: Prednisone, Azathioprine (Imuran), Cyclophosphamide (Cytoxan)

Guillain Barre
Plasmapheresis (Plasma exchange) Intravenous Immune Globin-use as immunosuppressant IVIg

Fractures - Crack or break in the continuity of a bone Classifications: Open Closed Complete Incomplete Types of Fracture Based on Mechanism of Injury- look at picture* - Normal, transverse, oblique, spiral, comminuted, segmental, avulsed, impacted, torus, greenstick Fractures Healing 1) Neonatal period o 2-4 weeks 2) Early childhood o 4 weeks 3) Later childhood o 6-8 weeks 4) Adolescence o 8-12 weeks Assessment look at table* Monitor for complications: - Compartment syndrome o Result from increase pressure in the tissue compartment leading to decreased perfusion to tissues and nerves o The five Ps: Pain, Pallor, Paresthesias, Pulses, Paralysis o Volkmanns ischemic contracture Result from unresolved compartment syndrome Ischemia causes degeneration and contracture of muscles - Fat Embolism Syndrome o Fat globule lodge in the pulmonary vasculature or peripheral circulation o Common in long bone fractures and major trauma o During first 12-72 hours post injury o Manifestations: Tachypnea, dyspnea, use of accessory muscles, wheezing, inspiratiory stridor Petechiae-neck, upper chest, shoulder, axillary and buccal membranes HA, drowsiness, irritability, memory loss, confusion, rapid pulse, apprehension, and fever - Deep Venous Thrombosis o Virchows Triad: Blood, Vessel, Flow Hypercoagulability, venous stasis, turbulent blood flow - Infection o Likely to occur in open fracture o May result from contamination at the time of injury or during surgery o Can result into delay healing and osteomyelitis o WOF: wound drainage, fever, pain, odor

Collaborative Care Therapeutic Management: - Cast, traction, closed reduction, open reduction, pharmacologic managements. Nursing Diagnosis: - Risk for impaired tissue perfusion, pain, impaired physical mobility, risk for infection, risk for impaired skin integrity Diagnostic Tests: - X-Ray, CT or MRI for discreet fractures, blood chemistry (renal functioning), CBC (bleeding), Coagulation studies (risk for clotting) Pharmacologic Treatments - Pain Medications, Narcotics, NSAIDs, Stool Softener Fracture Reduction 1) Closed Reduction (conservative) o For simple fractures o Bring the bone together by manipulation o Cast, Splint or Traction o X-ray post reduction 2) Open Reduction Internal Fixation (ORIF) (operative) o For complex fractures o Surgery o Reduction is achieved by through internal fixation 3) Mixed o Traction, cast, surgery, & electrical bone stimulator Traction - Application of a straightening or pulling force to return or maintain the realignment of the fractured bones. - Purposes: o Reduces fracture, lessen muscle spasm, correct deformity, relieves pain, promotes rest 1. Skin (straight) Traction o Traction is exerting its grabbing or pulling force through the clients skin. o Short term treatment 24 48 hours o Primary use is to control spasm o Immobilize the fracture before surgery Advantage Easy to use and ability to maintain comfort Disadvantage Weight required to maintain normal body alignment should not exceed the skin tolerance (6lbs) 2. Skeletal Traction o Application of pulling force through placement of pins into the bone. o Used to align bones or treat joint contractures Advantage More weights can be applied to maintain proper anatomical alignment (5 - 45 lbs) Disadvantage Increase risk of infection, Increased anxiety and discomfort. o Weights used in skeletal traction are not be removed. 3. Balanced Suspension Traction o Several forces work in unison to raise and support the clients injured extremity off the bed and pull it in a straight line away from the body. o Increases mobility without threatening joint continuity

4. Counter-traction o Pulling force exerted in a opposite direction to prevent the client from sliding to the end of the bed o Clients weight o Elevating foot of bed o Elevating head of bed for cervical traction Nursing Responsibilities for Patients in Traction Skin Traction - May remove weights only when intermittent traction has been ordered to alleviate muscle spasm - Assess skin integrity - Protect pressure sites with padding or protective dressing - Neurovascular checks Skeletal Traction - Never remove weights - Skin assessment and pin care as per policy - Report signs of infection - Pain management - Neurovascular checks Maintain counter-traction & line of pull, Do not wedge the clients foot or place it flush with foot board of the bed, Weight should be hanging freely, Avoid knots at the end of the rope to come in contact with the pulley, Place patient in the center of the bed, Frequent neurovascular checks, Assist in repositioning , Stabilize fracture while repositioning, Encourage use of over head trapeze, Assess for complications of immobility, Pressure sores, DVT, Pneumonia, ileus, renal stones, constipation Cast -

Rigid device applied to immobilize the injured bones and promote healing. For relatively stable fracture Maybe plaster or fiber glass applied over a thin cushion of padding o Plaster may take 48 hours to dry o Fiber glass will take 1 hour to dry

Nursing Responsibilities for Patients with Cast Frequent neurovascular checks, Assess for 5 Ps, Palpate cast for hot spot, Report any drainage promptly - Teach the patient: Not to put anything in the cast, If made of plaster keep it dry, If fiber glass cast becomes wet dry it with blow dryer in a cool setting, Use blow dryer on cool setting to relieve itching, Crutch walking Complications of Traction & Cast Pin-site infection, impaired circulation, Nerve damage, Pressure areas, Skin lesions, Tissue necrosis, Compartment Syndrome Surgery -

For fractures requiring direct visualization & repair Fracture with common long term complications Severely comminuted fracture Threatens blood supply o External Fixation Consist of a frame connected to pins that are inserted perpendicular to the long axis of the bone Increases independence while maintaining immobilization of the fracture Check for signs of infection and frequent neurovascular checks

Open Reduction Internal Fixation (ORIF) Implants inside the body Screw, wires, plates, intramedullary nail: usually for the shaft

Complication of external & internal fixation - Infection, Implant failure, Re-fracture, Non-union: if there is a gap between the ends of bone Nursing Responsibilities for Internal Fixation - Frequent neurovascular checks (5 Ps) Assess: - Bleeding, Wound for drainage, Hemovac drainage, Bowel sounds, Lung sounds - Encourage early ambulation & DBCE, Assist in weight bearing, Pain medication as ordered, Pin Care, Prevention of constipation, DVT PREVENTION Electrical Bone Stimulation - Electrical stress increases the migration of osteoblast and osteoclast to the fracture site. - Painless method of treating fracture that are not healing appropriately - 3 to 10 hours a day Hip Fractures Types: Intracapsular: (Subcapital & Transcervical); Extracapsular: (Intertronchanteric & Subtrochanteric) Signs and Symptoms: Pain, Inability to walk, Shortening of legs, External rotation of affected extremity, Internal rotation or displaced posteriorly Atypical Symptoms - Vague pain: Buttocks, Knees, Groin, Thigh - Ability to walk is unaffected Interdisciplinary Care Diagnostics: X-Ray, MRI & Bone scan Treatment: Traction to relieve spasm, Surgery within 24 hours, ORIF Fracture in Trochanteric area, Hemiarthroplasty & Total Hip Arthroplasty Fractured femoral neck Amputation - Removal of an extremity or part of an extremity - Reasons: Circulatory disorders, PVD, DM, Traumatic injury, Malignant tumors, Uncontrolled infection, Gangrene, Severe thermal or crushing injuries, Congenital deformities Types of Amputation Guillotine - When there is infection Closed - Flaps of muscle or tissue Complications: Infection, Greater risk in traumatic amputation, older, DM, and PVD. Delayed Healing- Due to infection, poor nutrition, electrolyte imbalance, smoking, & decreased blood flow. Phantom Pain- Aching, knifelike, jabbing, throbbing, tearing, burning pain in amputated part

Post- Op Nursing Care - Assess for hemorrhage and signs of infection - Pain Control - Teach care for the residual limb: o Wash daily with warm water and bacteriostatic soap, rinse and pat dry. o Expose to air about 20 in after washing; avoid using powder, lotion, alcohol & oils unless prescribed. o Change limb sock daily and discard socks that is in poor condition o Teach to do active ROM on other extremities - Prevent edema o Avoid dangling stump over bed o Elevate limb for the 1st 24 hours - Prevention of hip contractures o Lay prone for 30 minutes 3-4 time a day o Avoid elevating or sitting with residual limb on pillows to prevent flexion contractures - Prevent external rotation and abduction contractures o Correct alignment in bed o Place rolled towels or sand bags when in chair prevent external rotation - Assess types of dressings o Application of prosthesis immediately o Cast/rigid dressing o Elastic wrap dressing o ACE bandage for conical shape & decrease edema; wrap distal to proximal o Push skin into soft then gradually to harder surfaces Mobilizing - Practice in transferring, standing and early walking with crutches supervised. - Use of the PPAM (pneumatic device) aid, inflatable tube in metal frame with rocker foot o Early ambulation, Decrease swelling , Improve morale, Can be used as early as 2 weeks post-op Prosthetics OSTEOPOROSIS Description: - A Metabolic disorder characterized by low bone mass and micro-architectural deterioration of bone tissue (porous bones), with a consequent increase in bone fragility and susceptibility to fracture. - Look at picture: *Loss of trabecular plates (right) results in weakened bone structure significantly increasing risk of fractures. Risk factors - Family history, Increasing age, Being female, Being Caucasian or Asian , Being thin or having small body frame, Menopause, Low testosterone level in men, Diet low Ca+ and Vit D intake, Sedentary lifestyle, Medications: Antiseizure & steroids, Smoking and alcohol Description - Most prevalent among postmenopausal woman but can occur at any age and sex o 1 in 2 women and 1 in 4 man over age 50 will have an osteoporosis related fracture. Women have smaller body frame Bone resorption occurs earlier in women Breast feeding and pregnancy deplete calcium reserve

Women live longer than men, longevity increases risk for osteoporosis

Bone mass o How much bone mass is achieved between ages 25 35 & how much bone mass is lost later Fracture 1.5 million fracture per year: 700,000 vertebral, 300,000 hip, 250,000 wrist, 300,000 at other sites - Vertebral collapse can occur with little or no stress o Height loss, Kyphosis, Low back pain: As vertebra collapse it puts pressure on nerves causing pain that radiates to flank and abdomen Bone Scan - Technique used to create images of bone using small amount of radio active material that travels through the blood stream - Increased radio contrast absorption in osteomyelitis, osteoporosis, fracture, cancer of the bone, & Pagets disease Bone Mass Density (BMD) - Reduction bone mass >2.5 SD below the mean for young healthy adults = osteoporosis - Osteopenia: reduction by 1-2.5 SD. - Types of BMD testing : o Dualenergy x-ray absorptiometry (DXA or DEXA). Diagnostic Gold Standard Measures BMD in spine, hip, or wrist These are common sites for osteoporotic fractures Completed in a few minutes Considered to be highly accurate o Ultrasound densitometry Measures BMD in heel, patella Cost-effective Not as sensitive as DEXA Accurate enough for screening purposes Lab tests - Serum Alkaline Phosphatase (AST) o High in fracture o Normal in Osteoporosis - Glaprotien (osteoclastin) o Marker of osteoclastic activity o Reflects bone turn over - PTH o Maybe high or normal - Urine o Hypocalciuria may reflect malabsorption of calcium (therefore may have more calcium in stool but this is not typically measureable)

Nursing Diagnoses: Pain, Impaired physical mobility, Risk for injury, Impaired nutrition: less than body requirements Planning & Implementation :Provide client teaching regarding prevention, Teach the importance of proper nutrition to ensure adequate calcium intake, Dairy products contains calcium: Low-fat dairy products if there are concerns with weight gain. Some fats in dairy products aid in calcium absorption. Milk and milk products are the best source of calcium

Suggest alternative sources for lactose intolerance: Sardines, clams, oysters, salmon. Dark, green leafy vegetables: Broccoli, Collard green, Spinach, Bok Choy. What about vitamin D? - Teach about calcium supplements o Calcium carbonate Generic = 200-600mg Caltrate = 600mg TUMS Ultra = 400mg o Calcium Gluconate provide lower amount of elemental calcium that carbonate o Calcium citrate Not affected by gastric pH Teach about the importance of taking calcium supplement with vitamin D Vitamin D (400-800 IU) Calcium Requirements - Provide information regarding recommended daily dietary intake of calcium: Children 800 Up to age 24 1200-1500 Pregnant & breast feeding 1200-1500 Women 25 50 (premenopausal) 1000 Women over 50 (Postmenopausal) Taking ERT 1000 Not taking ERT 1500 Men 25 to 65 1000 Men over 65 1500 Planning & Implementation - Teach client about importance of regular weight bearing exercise, Jogging, dancing, walking (20 min 4 or more times a week)-Prevents and slows bone loss. Swimming and pool aerobics are NOT beneficial WHY???-Not weight bearing - Teach importance of Smoking cessation - Teach to avoid excessive intake of alcohol - Implement fall prevention Pharmacotherapy - Estrogen replacement therapy, Selective estrogen receptor modulator (SERM), Bisphosphonates, Calcitonin Estrogen Replacement Therapy (ERT) Indication: - Used to prevent and treat osteoporosis, For surgical menopause before age 50 Mechanism: - Decreases osteoclastic activity & increase osteoblastic activity Dose: - Estrogen: 0.625mg qd, 0.3mg - Progesterone 2.5mg qd (if uterus present) - Estrogen alone increases risk of endometrial cancer

Advantages - Increases bone density, Decreases risk of fracture, Relief of hot flashes, vaginal dryness, Decreases LDL, increases HDL Disadvantages - Increased risk of uterine ca (if unopposed), Increased risk of DVT, Possible increased risk of breast & endometrial cancer Selective Estrogen Receptor Modulators (SERM) Indication: - Treatment and prevention of osteoporosis by mimicking estrogen beneficial effects on bone density. Mechanism: - Decreases bone resorption Dose: - Raloxifene (Evista) 60mg qd Advantages - Increases bone density, Decreases fracture risk, No stimulation of breast or endometrial tissue, Decrease LDL Disadvantages - Increased risk of DVT, Not for women with history of blood clots, Doesnt treat post-menopausal symptoms, May increase hot flashes, No effect on HDL Bisphosphonates Approved agents: Alendronate (Fosamax) 5 70 mg once a week dosing Risedronate (Actonel) 5 30 mg once a week dosing Ibandronate (Boniva) 150 mg once a month Primidronate (Aredia) & Zoledronic (IV preparation) Indications: - Prevention & treatment of osteoporosis in post menopausal women, Prevention & treatment of steroid-induced osteoporosis both in men & women, Pagets disease , Hypercalcemia of malignancy Mechanism of Action - It adsorbs to hydroxyapatite and become a part of the bone structure. Bisphosphonates prevent bone resorption by inhibiting osteoclast activity, Prevent attachment of osteoclast to bone. Decrease the activity of osteoclast . Nursing responsibilities: - Take on empty stomach, Take first thing in morning (30 min before meal), No food or other meds 30 minutes after taking Bisphosphonates, Take with 8oz glass of water only, Remain in an upright position for at least 30 minutes after taking the drug - Biphosphanates result in esophagitis and GIT distress. Instruct to report chest pain of dysphagia - Separate Ca, Al, and Mg containing meds by at least 4 hours Advantages - Increases BMD, Decreases fracture risk by, No increased risk of breast, uterine ca or thromboembolic events Weekly or monthly dosing Disadvantages - Risk of gastrointestinal disorders, Contraindicated in renal failure; need to adjust dose according to creatinine clearance

Calcitonin - Principal effects are to lower serum calcium and phosphate Salmon calcitonin (Miacalcin, Calcimar) Nasal Spray - It inhibits osteoclast activity, decrease bone resorption thus lowers serum calcium and phosphate and reduce bone pain. It increase BMD in spine Indications: Pagets disease of bone, Osteoporosis, Hypercalcemia Side Effects: - Sore, Itching, Rhinitis, Transient ANV, urinary frequency, flushing of face, palms and soles of feet, IV risk of anaphylaxis Nursing Responsibilities: - Instruct to consume adequate amount of Calcium and Vit D, Take in evening to limit side effects, Warm to room temperature before using , Instruct to use alternate nostril each use, Instruct that ANV may occur during start of treatment, Instruct to report if nose bleed occur Arthritis 1) Osteoarthritis - Also known as Arthrosis or Degenerative Joint Disease (DJD) - Chronic disease causing deterioration of the joint cartilage - Bone rub against each other causing pain and decrease function - Formation of new bone (bone spurs/Osteophytes) at the margins of the joints forcing the bones out of their normal position and causes deformity. - Injury is limited to joint and surrounding tissues - Usually Monoarticular Joints Affected: Commonly affect hands and weight bearing joints. Hips, Knees, Hands, Spine, Big toes Risk factors: Age middle age to older (most significant), Obesity, Repetitive joint injury (sport, work-related, accidents), Sex - knees and hands osteoarthritis is more common and severe in women, Genetics most commonly OA of the hands Assessment - Physical exam and history of symptoms. Pain and stiffness in one or more joints. Weight bearing, Pain is described as deep ache, Pain is aggravated by motion and relieved by rest, Pain maybe localized or referred and accompanied by paresthesias. Stiffness is apparent after long period of immobility. Decreased ROM and grating or crepitus maybe noted as disease progresses. Joint enlargement, Flexion contractures - Toes-Eventually the toe may become stiff (hallux rigidus), which makes walking difficult. Bent (hallux valgus), which can lead to painful bunions. Hands: Heberden's nodes - Raised bony growths over the distal interphalangeal joints. Bouchards nodes - Raised bony growths over the proximal interphalangeal joints - Spine: Spondylosis, Degenerative Disk Diseases, Localized pain and stiffness, Muscle spasm, Limited ROM, Nerve compression causing weakness - X-Ray confirms the disease: Test for inflammation will be normal Collaborative care Therapeutic Regiment - Pharmacologic treatment: Acetaminophen, NSAIDs, Glucocorticoids: Maybe injected directly into the joint (Not more then every 4 6 months) - Joint replacement: Arthroplasty

Nursing Diagnosis - Impaired physical mobility, Self care deficit, Disturbed self image, Imbalanced nutrition more than body requirement Planning and Implementation: Encourage to participate in exercise program approved by healthcare provider, Encourage to maintain ideal body weight, Heat and cold compress for temporary relief, Encourage balance between rest and exercise, Rest Joint cane, crutches, walker, Assist with ADLs 2) Rheumatoid Arthritis Etiology & Pathophysiology: A form of autoimmune disorder. Associated with the deposition of antigen-antibody complexes. A systemic disorder involving symmetrical inflammation of synovial membranes. Females are 3x more likely than men to develop the disorder. Chronic disorder characterized by remission and exacerbation Assessment: Client usually present with Fatigue Anorexia Weight loss & General malaise, Persistent joint pain lasting > 3 months is more evident on motion, Morning stiffness lasting > 1 hour, Joint tenderness & swelling, Usually symmetrical As disease progresses characteristic deformities appear Labs - Positive RF (Rheumatoid factor - not specific) - Elevated ESR, C-Reactive protein, and serum complement - X-ray may show narrowed join spaces and erosive changes at bone margins - Synovial fluid will be cloudy, presence of WBC, and increased protein Collaborative Care - Therapeutic Management: Goals-Manage pain, Reduce inflammation, Preserve function, Prevent deformity, Pharmacologic treatment - Acetaminophen, NSAIDs, Glucocorticoids - Joint replacement: Arthroplasty Nursing Diagnosis: Pain, Self-Care Deficit, Altered Mobility, Risk for Fall, Disturbed Body Image, Activity intolerance related to chronic fatigue Planning and Implementation: Teach to modify schedule to include rest period, Medicate as ordered to relieve pain and modify the disease. Teach about drug side effects and potential interactions. Heat and Cold application to relieve pain Teach how to use assistive devices - Pharmacologic Management o Disease Modifying Anti-rheumatic Drugs (DMARD) Used to alter the rate of disease progression when NSAIDs are ineffective Examples: Gold Salts, Hydroxychloroquine (Plaquenil)-Base line eye exam and every 6 months Sulfasalazine (Azulfidine) & D-penicillamine (Cuprimine) o Immunosuppressive agents Azathioprine (Imuran), Cyclophosphamide (Cytoxan), Methotrexate (Rheumatrex) o Biologic Immunosuppressants

3. Gouty Arthritis Pathophysiology - Primary gout o Hereditary Elevated serum uric acid caused by inborn defects in purine metabolism Inherited defects resulting to a decreased renal tubular secretion of uric acid due to unknown cause. - Secondary gout o By the effects of certain drugs. Increased turnover of nucleic acids. Defects in renal excretion of uric acid salts. Prolonged fasting and excessive alcohol intake Risk factors: Obesity, Excessive alcohol intake, Impaired renal function, Hypertension, Drugs: Chemotherapy, Thiazide diuretics, Aspirin, TB drugs Assessment: Joint inflammation is extremely painful, polyarticular, Usually the metatarsal joint of the great toe, Red, hot, swollen, and tender joint. May have fever Labs: -

Uric Acid - Usually above 7 mg/dl CBC - Mild leukocytosis in acute attacks ESR & C-Reactive Protein might be elevated Analysis of fluid aspirated from inflamed joints o Show typical needle-shaped urate crystals o Provides the definitive diagnosis of Gout

Complications: - Tophaceous (Chronic) Gout o When hyperuricemia is not treated o Tophi : present joints, tendons, bursae, heart, or spinal epidural. Ulceration of tophi with chalky discharge - Genitourinary: o Uric crystals may deposit in the renal pelvis, collecting tubules, o Renal Stones can potentially obstruct urine flow and cause acute renal failure Collaborative Care Therapeutic Regimen Goal Terminate acute attacks Control of pain and inflammation Prevent future attacks Reduce serum uric acid levels Pharmacotherapy NSAID Corticosteroid Cholchicine

Allopurinol Joint replacement Arthroplasty Nursing Diagnosis Pain Impaired physical mobility Ineffective health maintenance Planning and Implementation Teach Dietary modification Low fat & low cholesterol diet Fasting is contraindicated WHY? Increase fluid intake (3 liters per day) when taking medications Avoid foods that are high in purine Turkey, organ meat, sardines, smelts, mackerel, anchovies, herring , bacon, beans, lentils, spinach, asparagus, mushrooms, cauliflower, oatmeal, ETOH, legumes Teach to avoid of Alcohol Consumption can increase uric acid production. Inhibits uric acid excretion in the kidney

Pharmacotherapy Colchicine Anti-inflammatory effects limited to gout Inhibits crystal-induced production of chemotatic factors Side Effects PO - Abdominal cramping, diarrhea, nausea, vomiting IV - Local pain, DIC, tissue damage on extravasation Contraindications - Significant GI, renal, hepatic or cardiac disease Question A patient with an acute attack of gout is treated with colchicine. The nurse knows the drug is effective upon finding Pain relief Pharmacotherapy Urate Lowering drugs Goal is for serum urate concentration to be at 6mg/dL or less Xanthine oxidase inhibitors Allopurinol (Zyloprim): blocks conversion of xanthine to uric acid. Start at lower doses with renal impaired patients Uricosuric drugs Probenecid or Sulfinpyrazone: increase renal clearance of uric acid by inhibiting tubular absorption Side effects may prohibit use - GI and kidney stones

Pharmacotherapy

Avoid use of medications that contribute to hyperuricemia: Thiazide and loop diuretics Low-dose salicylate Niacin Cyclosporine Ethambutol

Definition Hyperparathyroidism Increased release of PTH from the parathyroid gland. PRIMARY: hyperplasia or adenoma of the parathyroid gland SECONDARY: gland enlargement due to chronic hypocalcaemia in the presence of elevated PTH. (Chronic hypocalcaemia) TERTIARY: hyperplasia of parathyroid and loss of response to serum calcium levels (often in chronic renal failure) Nursing Diagnosis: Risk for injury Pain Impaired physical mobility Risk for altered urinary elimination Risk for constipation Knowledge deficit

Assessment/Risk Factors *2x more common in women -Health history -Vital signs -EKG -Elimination pattern -Nutrition status -Activity intolerance -Cognitive-perceptual and sensory function -Neuromuscular function

Symptoms -Polyuria -renal calculi-maintain urine acidity to reduce kidney stone formation -Constipation -Nausea and vomiting -Abdominal pain from peptic ulcer disease -Generalized bone pain -Pathologic fractures-less calcium in bones--caution with ambulation -Muscle weakness-deep tendon reflexes -Dysrhythmias -CNS signs: depressed DTR, paresthesias, depression, psychosis

Lab Tests Elevated total serum calcium. Normal values 911 mg/dL or 4.5-5.5 mEq/L Increased PTH. Normal values 11-54 pg/mL. Patient must be NPO for 8 hours Decreased Phosphate Possible bone changes on x-rays and CT scan

Management Decrease serum level of calcium: -IV normal saline infusion and increase fluid intake. -Low calcium diet -Minimally invasive parathyroidectomy -Medications to reduce calcium Planning/Implementation: Promote comfort and safety-prevent fall, may need walker-risk for osteoporosis Strain urine-risk for stones Increase OFI 2000-3000 ml/day Increase fiber in diet (constipation) Encourage activity as tolerated, pace activity with rest period Promote nutrition, and fluid and electrolyte balance Weigh daily Prevent tetany caused by surgery or aggressive excretion of calcium-from hypocalcaemia Early detection of low serum calcium-watch for numbness around the mouth and finger tips, muscle twitching, change in voice. Chvostek-cheek facial twitching and Trousseau sign: BP cuff, curl up hand

Medications Biphosphanates: bind to bone and inhibit calcium resorption from the bone. Pamidronate (Aredia), Alendronate (Fosamax), Risedronate (Actonel) Salmon Calcitonin (Miacalcin) Diuretics Phosphate replacement ERT-protects against bone loss and subsequent hypercalcemia

Definition Hypoparathyroidism Abnormally low levels of PTH. Usually due to inadvertent removal during parathyroidectomy. Results in hypocalcaemia and elevated blood phosphate levels (hyperphosphatemia) Nursing Diagnosis: -Deficient knowledge: calcium and vitamin D intake Deficient knowledge: disease process and drug therapy Risk for injury: tetany, sedation, seizures Risk for injury: hypercalcemia/hypocalcaemia

Assessment/Risk Factors Hypocalcaemia: raises excitability threshold of nerves and muscle fibers causing fibers to be easily stimulated. Could lead to life threatening tetany. Must have calcium gluconate at the bedside!

Symptoms GI symptoms: abdominal pain, anorexia, nausea and vomiting, diarrhea Signs of hypocalcaemia: anxiety, headache, neuromuscular irritability (Tetany)-parathesias or numbness around mouth and finger tips. Possible changes in voice, difficulty swallowing and sensation of tightness in throat. Chvosteks sign/Trousseaus sign, seizure, coma, death Dry, thin, hair, alopecia areata, ridged finger nails

Lab Tests Decreased PTH Increased Serum Phosphate

Management Increase serum calcium level Nutrition consult Supplemental calcium and vitamin D High calcium diet Calcium gluconate Planning/Implementation: Medic Alert bracelet Promote comfort and rest Prevent falls, may need walker Teach about signs of tetany Encourage activity as tolerated Pace activity with rest period Promote nutrition and fluid and electrolyte balance Teach about foods high in vitamin D Teach about foods high in calcium: cheese, milk, turnip greens, almonds, beans, frankfurters, and bologna. *Dont take turns several times a day-impairs absorption and wont absorb well.

Medications Goal is to increase serum calcium level. Must have calcium gluconate at bedside. Nutrition consult. Supplemental calcium/Vitamin D. Restore calcium balancehigh calcium diet.-no more than 2500 mg/day. 10% calcium gluconate 1020 mL IVP for emergency May need continuous IV gtt. May require adjunctive vitamin D (if calcium supplement alone is inadequate) no more than 400 IU per day. *Must be cautious if patient is on digoxin! add more calcium-increased contractility-may need to decrease digoxin.

Secretion of parathyroid hormone (PTH) increases the level of calcium in the blood. This increases resorption of calcium from filtrate (urine). Increasing calcium absorption in the gut. Increasing release of calcium from the bone. Secretion of calcitonin by the thyroid gland. This decreases the level of calcium in the blood. Pituitary gland: remember the pituitary gland is actually 2 glands: The anterior pituitary gland or adenohypophysis is a classical gland composed predominantly of cells that secrete protein hormones The posterior pituitary gland or neurohypophysis is not really an organ, but an extension of the hypothalamus. It is composed largely of the axons of hypothalamic neurons which extend downward as a large bundle behind the anterior pituitary.

Definition Hyperpituitarism (Anterior) Characterized by increased production of one or more tropic hormones. Most common caused by benign adenoma.

Assessment/Risk Factors

Symptoms Visual changes Increased Growth hormone, Prolactin, ACTH or TSH

Labs

Management -Irradiation of the pituitary gland. -Trans-sphenoidal (nose) /transfrontal adenohypophysectomy (lip) *Radiate or take out. Between eyes, behind frontal sinus in brain. Will need supplemental hormones

1)Gigantism/Acromegaly (Excessive GH) 2) Cushings Disease (Increased ACTH-increased cortisol) 3) Secondary Hyperthyroidism (Increased TSH)-increased metabolic rate 4) Hyperprolactinemia Female: decreased libido, irregular or absent menses, difficulty becoming pregnant Male: Decreased libido, gynecomastia, galactorrhea, impotence

Medications Nursing responsibilities: -Monitor vital signs as per unit policy -Assess LOC -Instruct to avoid coughing, sneezing or constipation -Keep HOB elevated at least 30 degrees -Avoid brushing from 1 week to 10 days to avoid disrupting suture line -Monitor for bleeding -Monitor urine output -Instruct about the need for hormone replacement Ocreotide (Sandostatin) -GI side effects, Expensive

Definition
Hypofunction of the Anterior Pituitary Gland -Panhypopituitarism -Sheehans syndrome (autoimmune) Syndrome of Inappropriate AntiDiuretic Hormone (SIADH) [Posterior Pituitary] (Excessive ADH)-retain water, salt -retain more water, hypotonic plasma into cells edema Causes: Head trauma, pituitary surgery, malignant tumorscarcinoma of the lungs, leukemia, pancreatic cancer, Hodgkins disease Diuretics Barbiturates Anesthetics Nursing Diagnosis: Altered thought process Acute pain Imbalance nutrition less than body requirements Fatigue Deficient knowledge

Assessment/Risk Factors

Symptoms
-Secondary hypothyroidism -Secondary adrenal hypofunction -Changes in secondary sex characteristics and sexual functions

Lab Tests

Management

Medications
Hormone replacement

Characterized by high levels of ADH in the absence of serum hypo-osmolality Water intoxication Cellular edema Dilutional hyponatremia General manifestations of fluid volume excess: excess ADH increases renal reabsorption of water into the circulation. -Increase in BP -Crackles on auscultation -JVD -Taut skin -Intake greater than output Identification of those at risk: those who have had intracranial trauma, surgery, and those who have tumors or infections (meningitis) Assessment of the patient who has had surgery or is susceptible to the syndrome is necessary for early detection. Be alert for: low urine output, high specific gravity, weight gain, serum sodium decline Implement fluid restriction to prevent further hemodilution.-frequent oral hygiene, ice chips or sugarless chewing gum can decrease thirst

As plasma volume continues to expand and serum sodium levels continue to decline cerebral edema occurs: (Fluid overload and electrolyte imbalance)-fatigue -anorexia and nausea -weight gain without edema -muscle aches -abdominal cramps and diarrhea (Water intoxication)-headache -lethargy -confusion -seizures -coma and possibly death if untreated (increase in water in CNS)

Diagnostic Findings: -Excess ADH increases renal reabsorption of water into the circulation. Serum osmolality declines (<275 mOsm/kg H2O) Low urine output (concentrated) -high urine osmolality (>1200 mOsm/kg H2O) -high urine specific gravity (>1.032) Sodium levels decline: <135 mEq/L (dilutional hyponatremia) Decreased hematocrit (hemodiluted) and BUN

If symptoms are mild and serum Na+ >125 mEq/L: -The only treatment may be fluid restriction of 800-1000 ml/day. This restriction should result in a gradual daily reduction in weight. A progressive rise in serum sodium concentration and osmolality, and symptomatic improvement Severe SIADH with serum Na+ <120 mEq/L: -risk for seizure! * -Fluid restriction of 500 ml per day may be necessary. -3-5% saline solution (hypertonic) is administered IV -Diuretic therapy may be indicated to promote dieresis Furosemide (Lasix)

Chronic SIADH: water restriction of 800-1000 ml/day is recommended If this is not tolerated two medications may be used: Buthorpanol (opioid) -inhibits ADH secretion and is useful in central nervous system causes of SIADH Demeclomycin (tetracycline antibiotic) -causes nephrogenic diabetes insipidus and blocks the action of ADH at the level of the distal and collecting tubules regardless of ADH source (causes kidneys to ignore ADH) *Monitor urine output to assess for effectiveness!!

During Acute Phase of SIADH:

No free water and flush gastric tubes with NS instead of H20. Monitor VS on acute episode. Accurate I &O monitoring. Daily weight (2lbs = 1 liter of fluid) Monitor for signs of improving or worsening fluid retention

Weight, heart sounds, lung sounds. Monitor serum sodium, urine osmolality, and specific gravity. Neuro assessment. Elevate HOB to not more than 10 degreesfool heart to secreting diuretic

Client education: teach about SIADH and symptoms to report. About signs and symptoms of fluid overload. Weigh daily on same scale. Report 2lbs in a day.

Instruct to supplement diet with sodium and potassium. Medication maybe for life depending on the cause. If treated with Declomycin (nephrotoxic) monitor side effects and signs of fungal infection! *

Definition
Diabetes Insipidus (DI) Excessive loss of water caused by hyposecretion of ADH or the kidneys inability to respond to ADH. Polyuria ranging from 4-30 L in 24 hours can lead to dehydration if the client does not replace the lost water. 3 Types of DI: Neurogenic (Central) DI: -Occurs when any organic lesion of the hypothalamus infundibular stem, or posterior pituitary interferes with ADH synthesis, transport or release. Causes include: Brain tumor/closed head trauma, Pituitary or other cranial surgery, CNS infections Nephrogenic DI: Problem result from inadequate renal response to adequate presence of ADH. Can be hereditary, result from renal damage, or drugs such as lithium and declomycin Psychogenic DI: Result from excessive water intake which can result from structural lesion in the thirst center or psychological disorder

Assessment/Risk Factors
-Assess for history of head injury, brain injury, infection or tumor. -Obtain list of medications -Assess LOC: sensory disturbance, anxiety and restlessness, diminished alertness/cognition, coma (severe fluid volume deficit) *brain cells shrinking -Weight loss: >2% Mild FVD, >5% Moderate FVD, >8% Severe FVD -Cardiovascular: Orthostatic BP (Moderate FVD), falling SBP/DBP (Severe FVD), resting tachycardia, decreased pulse volume, hypovolemic shock Elevated body temperature Assess skin: diminished skin turgor, dry skin, dry mucus membrane Assess bowl sound: constipation (decrease fluid) Increase in sodium levels

Symptoms
Increased urination (polyuria)-excretion of large quantities of urine (5-20 liters/day) in milder form the urine may be only 2-4 liters per day Increased thirst (polydipsia) -dehydrated -client compensates by drinking large amouns of waer so that serum osmolality is normal or only moderately elevated Nursing Diagnosis: Fluid volume deficit r/t inadequate ADH Risk for impaired skin integrity Risk for injury r/t electrolyte imbalance Risk for constipation Dehydration

Lab tests
Urine specific gravity <1.005 Urine osmolality <300 mOsm/kg Serum sodium >145 mEq/L Low serum ADH level for central DI Positive water deprivation test Water Deprivation Test: Test to differentiate between central and nephrogenic DI Before test: weight, pulse, BP, urine and plasma osmolality, urine specific gravity, patient will be NPO for 8-16 hours During the test: BP, weight, and urine osmolality are assessed q1 hour The test continues until urine osmolalilty stabilizes: hourly increase is less than 30 mOsm/kg in 3 consecutive hours or body weight declines by 3% or orthostatic hypotension develops. ADH will then be given-urine osmolality is then measured after an hour. Central DI-a 9% rise in urine osmolality. Nephrogenic-DI-no response

Management
IV fluid: hypotonic saline or D5W give IV and titrated based on urine output Neurogenic DI: hormonal replacement-Desmopressin acetate (DDAVP) and analog of ADH. Synthetic vasopressin, can be given IV, PO, or nasally. Other preparation vasopressin (Pitressin) Diet: hormone replacement and chlorpropamide have little or no effect in treatment of nephrogenic DI. Low NA+ diet -3 grams per day-thick to retain water. Invoke RAAS. Planning/Implementation: -Encourage increase in fluid intake PO or IV: keep adequate amount at bedside. If IV glucose solution is used monitor serum sugarhyperglycemia can result into osmotic dieresis. -accurate I&O: report urine output >200 ml/hour 2 consecutive hours or 500 ml over 2 hours. Report sudden increase in urine output or a decrease in urine specific gravity. -monitor urine specific gravity, report if it decreases. -Daily weight-report weight loss -Monitor for signs of water intoxication

Medications
Carbamazapine (Tegretol)antiseizure and Chlorpropamide (Diabenese) These drugs are thought to potentiate the action of ADH and stimulate endogenous release. Chlorpropamide is considered to be most consistently effective and safest. Thiazide Diuretics-Promote Na+ loss. Invoke the RAAS Indomethacin (Indocin)-is a NSAID that has the ability to increase renal responsiveness to ADH Teaching: -about DI and to wear medic alert bracelet listing DI and treatments -instruct to drink fluid equal to urine output (keep log) -teach self administration of medication: may be life long, alternate nostrils, teach about drug side effects and toxicities, how to assess effectiveness of treatment -daily weight and report weight loss -low sodium diet -consult practitioner before taking OTC medications

Definition
Hyperthyroidism A sustained increase in synthesis and release of thyroid hormones (T3 & T4) by thyroid gland resulting to increased BMR. Can be caused by: increased secretion of thyrotropin (TSH) from pituitary -Secondary -Autoimmune (Graves Disease) Primary-low TSH -Inflammation or viral infection of the thyroid gland (Thyroiditis) -tumor -Excessive supplementation of thyroid hormone Nursing Diagnosis: Risk for decreased cardiac output Disturbed sensory perception (visual)-exothalamus Risk for ineffective airway clearance Goiter Hyperthermia-heat intolerance -activity intolerance HR, decreased CO, increased BMR -Risk for imbalanced nutrition less than body requirements: increased BMR

Assessment/Risk Factors
Related to effect of thyroid hormone excess: -increased tissue sensitivity to stimulation by sympathetic nervous system. -Increased BMR -Intolerance to heat -elevated basal temperature -weight loss -fluid volume deficit ***Know chart on slide. Ophthalmopathy: Abnormal eye appearance or function. -Exophthalmos-Graves disease has it too. Protrusion of eyeballs from the orbits. Increased fat and edema in retroorbital tissues. Seen in 20-40% of patients with Graves Disease. Patient may require eye care. risk for corneal abrasion. (Antibodies cause increase in mass behind eye) Thyrotoxic crisis Thyroid Storm: Life threatening emergency occurring in extreme hyperthyroidism. Death rare when treatment initiated. Occurs in long term untreated hyperthyroidism. Presumed causes are additional stressors: infection, trauma, manipulation of thyroid gland.

Symptoms
Toxic Nodular Goiter: -occurs equally in men and women. -usually benign follicular adenomas -multiple or single nodules -thyroid hormones-secreting nodules independent of TSH -IF associated with hyperthyroidism, termed toxic -can have difficulty swallowing and bruit is present Manifestations of thyroid storm: -temp of >102 -systolic hypertension -nausea, vomiting and diarrhea -agitation -tremors -confusion and delirium -seizures, coma, death -heart failure -shock Teaching: Medication administration Symptoms of hyper and hypo Instruct to report signs of hemorrhage, hypocalcaemia, respiratory difficulty, incisional infection Support neck to avoid strain Wound care Limit coughing and strain talking -regular eye exam* Report changes in vision or appearance of eyes Eye pain, closure of eyelids Eye exudates, photophobia* Sleep with HOB elevated -protect eyes -artificial tears, eye patches

Lab Tests
TSH: PTG increased or TG decreased. Elevated free thyroxine (free T4) and total T3 (triiodothyronine) and T4 Radioactive iodine uptake (RAIU): indicated to differentiate Graves disease from other forms of thyroiditis. (fairly diagnostic) Drug Therapy: for decreasing size and vascularity of thyroid gland preoperatively. Useful in treatment of thyrotoxic states. Not considered curative. 1. Anti-thyroid Drugs: inhibit synthesis of thyroid hormone. First line anti-thyroid drugs: Propylthiouracil (PTU) blocks conversion of T4 to T3. Methimazole (Tapazole). Improvement in 1-2 weeks. Good results in 4-8 weeks. 2. Iodine.-used with other drugs. Prep for surgery or crisis. Decreases vascularity of thyroid gland. Inhibits synthesis of T3 &4 and blocks their release. Saturated solution of potassium iodine (SSKI) and Lugols solution. -*watch allergy to shellfish. 3. B-Adrenergic Blockers: symptomatic relief of thyrotoxicosis resulting from b adrenergic receptor stimulation. Propanolol (Inderal) administered with other drugs. Decreases Heart rate.

Management
Preoperative thyroidectomy: -Teach DB and appropriate coughing. -Instruct to hold hand behind neck when coughing, sitting, turning or getting up/back to bed to reduce post op pain and neck muscle strain. -Instruct patient on self administration of prescribed anti-thyroid medication to decrease vascularity and size of thyroid to minimize risk of bleeding post surgery. Ensure client understands the procedure. Informed consent. Subtotal Thyroidectomy: preferred surgical procedure. Involves removal of significant portion of thyroid. 90% removed to be effective. IF too much is removed, regeneration will not occur. Results in hypothyroidism. Post op: provide comfortanalgesics, semi-fowlers position with head supported by pillow to prevent muscle strain, ice collar to wound for comfort and prevent edema. Maintain IV. Assess for laryngeal nerve damage. ability to speak loudly, quality of voice and tone. May have some speaking difficulty for a short time. Auscultate trachea for strider. Indicates edema of airway. Monitor for hemorrhage. 24 hrs after. Promote patent airway. HOB elevated. Keep suction by bed and tracheostomy tray.* deep breathing. WOF tetany. calcium gluconate. (may accidently remove Parathy.)

Medications
Ethionamide Drugs for life Ablative radioactive I-131 Thyroidectomy Partial or Radical -shrink thyroid before surgery to decrease risk of thyroid storm. *Increased calorie, increased protein diet, dairy productson exam Radioactive I-131: Administered as outpatient treatment. Not recommended for pregnant women. Radioactive precaution is not required for small doses (<30 mCi) of I-131. Instruct to drink solution with straw to minimize exposure of buccal cavity. Delayed response. 2-3 months: treated with antithyroid drugs and Inderal before and during the first 3 months of RAI. Swallow pill w/iodine thyroid gland: kill cells decreased production of T3 and T4. eventually risk of hypothyroidism. Give T4=synthroid. May cause dryness and irritation of mouth and throat. Relief includes frequent sips of water, ice chips, salt/soda gargle. Post treatment hypothyroidism: need for lifelong hormone replacement. Teach symptoms and instruct to seek medical help if symptoms occur.

Graves Disease

Hypothyroidism Results from insufficient circulating thyroid hormone causing decreased BMR, decreased heat production, and various effects on body system. PRIMARY: more common in women. Related to destruction of thyroid tissue by autoantibodies (Hashimotos thyroiditis) SECONDARY: central hypothyroidism. Related to pituitary disease with decrease in TSH secretion of APG or decreased TRH release from hypothalamus Nursing Diagnosis: Decreased cardiac output Hypothermia Constipation Risk for skin integrity impairment Risk for activity intolerance Risk for sexual dysfunction Disturbed body image

Most common form of hyperthyroidism. 7-10 times more common in women 20-40 years old. Autoimmune disease of unknown etiology -Antibodies are developed to TSH receptor causing long acting thyroid stimulator (LATS) causing excessive thyroid hormone secretion (Increased T3 & T4) Causes: Iodine deficiency: most common cause worldwide and is most prevalent in iodine deficient areas. Infection, external irradiation or surgery, iatrogenic, idiopathic Assessment: Health history, LOC and vital signs, respiratory effort, activity intolerance. Varies depending on severity of condition, duration and age of onset. Myxedema: can be precipitated by infection, cold, trauma, drugs

Diffuse thyroid enlargement (Goiter) Decreased TSH level Antibodies TSH receptor in thyroid gland increased stimulation Low TSH level: TG increases than TSH should decrease because T3 and T4 are too high. ***Know symptoms slide chart Myxedema: a life threatening crisis state of hypothyroidism. Those with severe and untreated longstanding hypothyroidism may display myxedema. Accumulation of hydrophilic mucopolysaccharides underneath the dermis and other tissues. -Non-pitting edema in connective tissues throughout the body. -Puffy face and tongue -severe metabolic disorder -hypothermia -cardiovascular change -coma (myxedema)

Serum TSH: determines cause of hypothyroidism. Maybe increased or decreased. -Primary its increased, secondary its decreased. Decreased serum T3 & T4 TRH stimulation test: Hypothalamic versus pituitary dysfunction. Increase in TSH after TRH injection suggests hypothalamic dysfunction. No change after TRH injection suggests anterior pituitary dysfunction. Stim TRH would increase TSH. No change = pituitary. Increase = hypothalamus

Restoration of euthyroid state as safely and rapidly as possible with medications. Adjust environment with blankets as needed for temperature of comfort. Chilling increases metabolic rate, cardiac workload and oxygen demand. -Pace activities with rest periods. Instruct to report SOB, fatigue, dizziness or discomfot. -Encourage intake of 2000 ml of water daily and high fiber diet. Promote regular bowel movement. Education: About disease, self management, medications, medic alert bracelet worn. -medicaiton should be taken for life and should be taken at the same time every morning 1 hour before meal or 2 hours after meal.* -Take same brand*

Hormone replacement: Thyroxine (Synthroid) T4 not active right away Triidothyronine (Cytomel) T3 active -Give medication in the morning 1 hour before or 2 hours after food intake to facilitate absorption. Monitor for angina and cardiac Dysrhythmias. too much. Monitor thyroid hormone levels. every 3 months Instruct to report: -weight gain or loss -activity intolerance -chest pain -heat or cold intolerance -sleep pattern disturbance

Definition Cushing Syndrome Disorder of the Adrenal Cortex Hyper-function of the adrenal gland cortex causing elevated cortisol. Can cause life threatening changes in physiological, psychological, and metabolic function. More common in women with onset 30-40 years old. Etiology: PRIMARY-adrenal tumors SECONDARY-Cushings disease (ACTH-secreting pituitary tumor) Ectopic ACTH production in tumors IATROGENIC- administration of exogenous corticosteroids *Increase in ACTH tells adrenals to release too much cortisol. Nursing Diagnosis: Fluid volume excessaldosterone, increased Blood sugar Risk for injury-osteoporosis, fractures Risk for infection-bone marrow suppression Disturbed Body Imageincreased central weight, muscle wasting Knowledge deficit

Assessment/Risk Factors Vital signs- decrease pulse and BP Activity intolerance Skin condition-thin, bruise easy Elimination patternconstipation Nutrition problem Fluid and Electrolytes Self concept-look will changeretain water. Limbs are skinny, trunk edema Frequency of blood sugar monitoring-cortisol causes elevated blood sugar. Elevated Serum Cortisol Elevated urine 17Ketosteroids Plasma ACTH may be low, normal, or elevated depending on problem. Cushings Syndrome: decreased or normal ACTH, increased cortisol. (negative feedback) Cushings Disease: Increased ACTH, increased cortisol (pituitarys fault)

Symptoms Elevated Cortisol: -Muscle wasting and fatigue: Catabolic effects of cortisol, thin extremities that bruises easy, poor wound healing. Bodies use muscle protein for energy-> wasting. Bruise easy from the breakdown of protein -weight gain: trunk (central obesity), face moon face, cervical area causing buffalo humps, weight gain from sodium and water retention, purplish red striae on abdomen, breast or buttocks. Buffalo hump=fat and sugar. Hyperglycemia: gluconeogenesis-create new sugar. Glucose intolerance associated with cortisolinduced insulin resistance. Prevents insulin from going into cells Psychological disturbance: mood disturbances, insomnia, irrationality, psychosis. Elevated Androgens (sex hormones): -pronounced acne, virilization in women, feminization in men. Women: menstrual disorder and hirsutism, men: gynecomastia and impotence

Lab Tests ACTH suppression test: Cortisol and ACTH level should decrease in response to administration of dexamethasone. -if it goes down, its secondary. This drug suppresses the anterior pituitary. CT & MRI of pituitary and adrenal glands. Associated findings but are not diagnostic of Cushing syndrome: -Hypokalemia -Lymphopenia-suppresses immune system -Hyperglycemia and glycosuria (above 200) -Hypercalcemia and hypercalciuria -Osteoporosis-side effect of steroids *At risk for infection, fractures, muscle twitching, Dysrhythmias, kidney stones

Management Primary goal is to normalize hormone secretion. Treatment depends on cause: -Medications to decrease ACTH or cortisol release. dexamethasone if secondary. -Primary adenoma-secondary. (surgical removal or irradiation of pituitary tumor) -Adrenal tumors or hyperplasia-Adrenalectomy Planning and Implementation: Assist client in maintaining fluid, electrolyte, glucose and calcium balance. Monitor daily weight and I&O. Promote Safety-uncluttered walking area, adequate lighting, assistive device, nonskid shoe/socks. Encourage verbalization of feeling. Reassure that symptoms will go away with proper treatment. Teach the patient about the planned surgical procedure, postoperative routines and expected outcomes. Post Adrenalectomy: Promotion of wound healing and monitor for bleeding. Risk for hemorrhage is increased because of high vascularity of adrenal glands. Manipulation of glandular tissue may release hormones into circulation. BP, fluid balance, and electrolyte levels tend to be unstable b/c of hormone fluctuations. Monitor fluid intake and output for imbalance. *High doses of corticosteroids administered by IV during and several days after surgery. increased risk of infection.

Medications Metyrapone, Ketoconazole, Aminoglutethimide-inhibit cortisol synthesis and secretion by the adrenal cortex. Sandostatin (Ocreotide)-only secondary. Somatostatin analogue that inhibits ACTH release. Mitotane (primary)-medical adrenalectomy-the drug causes destruction of adrenal tissue. Suppresses cortisol production. Prevention of Addisonian Crisis: WOF dryness, tenting skin, anorexia, weakness, hypotension, tachycardia, tachypnea, decreased LOC -Bolus of IV normal saline (0.9 NaCl) -IV cortisol (Methylprednisolone) Education: Teach about the disease process and importance of medic alert bracelet. Teach about post operative cortisol replacement. Instruct about symptoms to report. Instruct about wound care. Instruct to eat diet high in protein, Vitamin C and B to support immune system. May need to take supplemental potassium and calcium.

Definition Addisons Disease From treatment of Cushings normally. Insufficient level of cortisol because of destruction of the adrenal cortex. -autoimmune, TB, infarction, fungal infection, AIDS, Metastatic cancer, Iatrogenic Addisons disease may be due to adrenal hemorrhage. More common in women <60 years old. *Decreased cortisol and aldosterone Nursing Diagnosis: Deficient fluid volume Risk of ineffective therapeutic management Risk for electrolyte imbalance Deficient knowledge

Assessment/Risk Factors Decreased cortisol and aldosterone: -hyponatremia -hyperkalemia-dysrythmias -Decreased ECF and IVF -Decreased gluconeogenesis and hypoglycemia -Stress intolerance -need for steroids, increase levels of cortisol in stress. Vital signs, LOC, skin, energy level and activity intolerance (Increased respirations, increased heart rate, decreased BP), Orthostatic BP, ECG, nutrition pattern, elimination pattern

Symptoms Skin hyperpigmentation -Areas exposed to sun, over joints, in skin creases, especially palm creases. -Cardiovascular changes: tachycardia, Dysrhythmias, postural hypotension -dehydration and hypovolemia -weight loss -ANV -diarrhea -depression, confusion and lethargy -fatigue -decreased calcium Risk for life threatening Addisonian crisis caused by: -sudden sharp decrease or an increased need for adrenocortical hormone -triggered by any form of stress (infection, surgery, trauma, hemorrhage) -sudden withdrawal of corticosteroid replacement therapy -severe manifestations of glucocorticosteroid and mineralcorticoid deficiencies: severe hypotension, circulatory collapse, shock, coma Severe episodic hypertension Severe pounding headache Tachycardia with palpitations Profuse sweating Abdominal or chest pain

Lab Tests Subnormal levels of cortisol Decreased urine 17 ketosteroid ACTH stimulation test-level goes up, pituitary at fault. -Levels fall to rise over basal levels with administration of ACTH indicates primary adrenal disease (Addisons disease) Positive response to ACTH stimulation indicates fluctuating adrenal gland secondary CT and MRI used to locate tumors, identify adrenal calcifications or enlargement Other abnormal labs: -hyperkalemia, hyponatremia, hypoglycemia

Management Replacement of glucocorticoids and mineralocorticoids Planning/Implementation: Maintain fluid and electrolyte balance: analyze value, intake and output, daily weight, encourage increase fluid intake up to 3000 ml/day and added sodium in the diet. Prevention and management of Addisonian crisis: -Glucocorticoid doseage must be increased during times of stress. doubled for minor stressors and tripled for major stressors. Treatment directed at: -Isotonic IV, Inotropes, High dose hydrocortisone replacement

Medications Hydrocortisone (Cortef) given in devided doses Fludocortisone (Florinef)-only once in the morning. -probably given for life. Education: Teach about the disease process. About the need for lifelong medication and disease management. Self management of medication. Plan for medication adjustment targeting stress response. Instruct to consult practitioner before taking OTC medications. Importance of medic alert bracelet. Diet to promote immune function and foods to increase sodium and decrease potassium

Pheochromocytoma Mostly in young and middleaged adults. Caused by a tumor of the adrenal medulla. Adrenal medulla: -Norephinephrine-endocrine, slower response -Ephinephrine-nervous system

Produces excessive catecholamines: results in severe hypertension-risk for stroke. If untreated may lead to: diabetes mellitus (increase in cortisol), cardiomyopathy, stroke, MI, Renal failure, Death.

24 hour urine collection. -Metanephrines-breakdown of ephrines. -Vanilyl Mandelic Acid Plasma catecholamines are elevated. CT and MRI used for tumor localization

Surgical removal of tumor. Sympathetic blocking agents: -Alpha and Beta adrenergic blockers: -symptoms of catecholamine excess: Decrease in BP and Decrease in Dysrhythmias

Monitor BP closely, make patient as comfortable as possible. Monitor glucose. Patient needs rest, nourishment and emotional support, stress importance of follow up care, routine BP monitoring

Definition Diabetes Mellitus Diabetes is not a single disease. Rather, it is a heterogeneous group of syndromes characterized by an elevation of blood glucose caused by a relative or absolute deficiency in insulin. The ADA recognizes 4 clinical classifications of diabetes: Type 1 diabetes (formerly insulin-dependent diabetes mellitus) Type 2 diabetes (formerly non-insulin dependent diabetes mellitus) Gestational diabetes (GDM) 28 weeks check Diabetes due to other causes

Assessment/Risk Factors *Understand 2 charts in the PowerPoint **Know oral agents for insulin in the PowerPoint. Sulfonylureas Meglitinide analogs Insulin Sensitizers -Biguanides -Thiazolidinediones or Glitazones A-Glucosidase Inhibitors -Acarbose and Miglitol Amylin and Incretin Dipeptidyl Peptidase-IV inhibitors Synthetic Amylin Analog

Symptoms Adverse effects to insulin: -hypoglycemia (most serious and common adverse reactions) -lipodystrophy-rotate injection sites! -Weight gain -Allergic reactions

Lab Tests Normal Blood Glucose = 70110 mg/dL Diagnosis: Fasting Plasma glucose (FPG) > 126 mg/dL Random plasma glucose (PG): nonfasting >200 mg/dL with symptoms. (3 Ps) 2 hour plasma glucose: >200 mg/dL during the oral glucose tolerance test (normal <140 mg/dL) *10 hour NPO (Except water, 75-100 gm of glucose given; blood and urine samples at 30, 60, 120 mins after) Glycosylated Hemoglobin(A1C): determines average blood glucose levels over 2-3 months: Norm = <79%. Shows how well blood sugar is controlled. Increased blood sugar, then there is more attached to hemoglobin. Increased sugar increased A1C. *Know chart on criteria for diagnosis

Management Type 1: requires exogenous (injected insulin) to control hyperglycemia, avoid ketoacidosis and maintain acceptable levels of glycosylated hemoglobin Type 2: primary treatment is diet and exercise. Most patients are dependent on pharmacologic interventions with oral hypoglycemic agents. As the disease progresses, Beta cell function declines and insulin therapy is often required to achieve satisfactory serum glucose levels Treatment: injection of insulin twice a day. Mix regular and NPH. Intensive treatment: seeks to normalize blood glucose through more frequent injections of insulin. Frequency of hypoglycemia is higher.

Medications Human insulin: produced by recombinant DNA technology using special strains of E coli or yeast that have been genetically altered to contain the gene for human insulin. Insulin Analogs: modifications of the amino acid sequence of human insulin have produced insulins with different pharmacokinetic properties. -Lispro, Aspart, and Glulisine: faster onset and shorter duration of action than regular insulin -Glargine and Determir: long acting insulins and show prolonged, flat levels of the hormone following injection. Route: generally subcutaneous. Regular insulin can be given IV. DKA Hyperkalemia. Ultra fast/ultra short acting: lispro (Humalog), aspart (novalog), glulisine (Apidra) Short acting: regular Intermediate: NPH Ultra long acting: glargine (Lantus) /detemir (Levimir) *Know chart & length of time