MedSurg Medications & Tables

Inflammatory(Nonselective COX Inhibitors)Acetic Acid:DiclofenacEtodolacIndomethacinSulinclacTolmetin

Propinonic Acid:FenoprofenFlurbiprofenIbuprofenKetoprofenNaproxenOxaprozin

Fenamate:MeclofenamateMeclofenamic acid

Salicylate:AspirinDiflunisal

Naphthylalkanone:Nabumetone

Oxicam:PiroxicamMeloxicam

Choline magnesium trisalicylate:Salsalate

(Selective COX-2 Inhibitors)CelecoxibRofecoxib

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 ImmunosuppressantsAnti-thymocyte antibodies:OKT3 (Muromonab-CD3)Antilymphocyte GlobulinAntithymocyte Globulin-Rabbit

IL-2 Receptor Antibodies:Basilixmab (Simulect) Daclizumab (Zenapax)

Antihistamines: First Generation:DipenhydraminePromethazineBrompheniramineDiphenhydramineChlorpheniramineDexchlorpheniramineCyproheptadineHydroxyzineClemastinePromethazineTripolidine

Second Generation:AzlastineCetirizineDesloratidineLoratadineFexofenadine

Type 1 Hypersensitivity:Epinephrine Dopamine/Dobutamine

Type 2 Hypersensitivity: Blood & SalineDipenhydramine

Type 3 Hypersensitivity:Aspirin or NSAIDPlaqeunilSteroidsImmunosuppressants:Azathioprine (Imuran)Cyclophosphamide (Cytoxan)

Cyclophosphamide (Sandimmune)Mycophenolate (CellCept)

HIV:PCP:TrimethoprimSulfamethoxazle-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. Saquinavirb. Ritonavirc. Intinavir

3. Entry/Fusion Inhibitorsa. Enfuvirtide (Fuzeon)

4. Nucleoside reverse transcriptase inhibitors

a. Zidovudin AZT (Retrovir)

HAART

Others:Stavudin (Zerit)Lamividine (Epivar)Zidovudin (AZT, Retrovir)MarinolMegace

Fe Deficiency AnemiaOral Iron Salts: Ferrous sulfate, ferrous lactate, ferrous fumarateIV Iron Dextran

B12 Deficiency AnemiaVitamin B12 (Cobalamin) Injection

Folic Acid Deficiency AnemiaVitamin B9 Supplement

Aplastic AnemiaBlood transfusionBone Marrow transplantImmunosuppressive therapy

Sickle Cell AnemiaFolic Acid SupplementsBlood transfusionGenetic 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 PlasmapharesisTransfusion of platelets Splenectomy

TTP:PlasmapharesisCryosupernatant plasma & Solvent deterent plasmaDO NOT TRANSFUSE PLATELETS

HIT:NO HEPARIN OR HEPARIN PRODUCTSArgatrobanLepirudinFondaparinux (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)

CisplatinNitrosureas

Cell-Cycle Specific:Antimetabolites

- Methotrexate - 5 Fluorouracil- 6 Mercaptopurine

*Leucovorin RescueMitotic Inhibitors

- Vincristine- Vinblastine

Bleomycin AntibioticsVinca alkaloidsEtoposide

Hormones:Tamoxifen (Novaldex)FlutamideNilutamideBicalutamide

Immunotherapy:Monoclonal Antibodies

- Trastuzmab- Rituximab- Bevaxizmab- Cetuximab

BCG (Bacillus-Calmette & Guerin)

Drugs to Know: 1. Inflammatory Process

- NSAIDS- COX 2 Inhibitors- Leukotrien Inhibitors

COX 1PG12: 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 2PGE2 & PGF2a: Inflammation anti-inflammatory effectmonitor for efficacy, therapeutic

Nonselective COX InhibitorsAcetic Acid Propionic Acid Fenamate Salicylate Naphthylalkanone Oxicam Choline

magnesium trisalicylate

DiclofenacEtodolacIndomethacinSulinclacTolmetin

FenoprofenFlurbiprofenIbuprofenKetoprofenNaproxenOxaprozin

MeclofenamateMeclofenamic acid

AspirinDiflunisal

Nabumetone PiroxicamMeloxicam

Salsalate

Selective COX-2 InhibitorsCelecoxibRofecoxib

*Lesser side effects Don’t take if at risk for blood clots! Risks for clotting-HA, stroke, etc.

Aspirin- Salicylate NSAID

o Antipyretico Analgesico Anti-inflammatoryo 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 Function InhibitorCox 1 Organ pain, platelet function, stomach

protectionNSAIDs including aspirin

Cox 2 Inducible: inflammation, pain, fever NSAIDs, COX 2 inhibitors including celebrex

Cox 3 Pain pathways, not inflammation pathways

Acetaminophen & some NSAIDs

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 child…Avoid taking NSAIDs at all during the 3rd trimester. Prolongation of gestation and inhibitor of labor. Risk for Patent Ductus Arteriousus

2. ImmunosuppressantsCorticosteroidAdverse Effects:

- All commonly occur because high doses used for immunosuppression:o Cushing’s Syndrome

Hyperglycemia (Gluconeogenesis) Weight gain (Na & H2O retention) Abnormal fats distribution Hypertension Hypokalemia

o Gastric Ulcero Euphoric personality changeso Osteoporosis

Inhibition of osteoblastic activity, decreased calcium absorption, increased urinary calcium excretion

o Cataracts

Calcineurin Inhibitors : interleukin 2 production blockersCyclosporine (Sandimmune) Tracolimus (Prograft) Sirolimus (Rapamune)Adverse Effects:

- Nephrotoxicity- Hepatotoxicity- Hirsutism- Neurotoxicity- Lymphoma- Anaphylaxis

Drug Interactions:- Induction and inhibition of

hepatic cytochrom: P450- Nephrotoxic drugs- Grapefruit juice (inhibits

p450)

Adverse Effects: - Nephrotoxicity- Increased risk of lymphoma- Hypersensitivity- GI complaints- Hypertention

Drug Interactions:- Agents that inhibit CYP3A (an

isozyme of cytochrome P450)- Grapefruit juice- NSAIDs

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 AgentsT-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 & Uses1. Blocks all T cell function2. Inhibits cytotoxic T killer cell function3. Opsonizes circulating T lymphocytes and enhances their removal

a. Depletes T cells prior to bone marrow transplantb. 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 Globulin3) Antithymocyte Globulin-Rabbit- Used to treat acute rejection transplant- Mechanisms

o Removal of T cells from circulationo Decrease cytokine induced reactions

- Adverse Effectso 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 functiono Baseline CBCo 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 Masko Use of strict aseptic technique in caring for IV lines, urinary catheter & wound careo 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 transfusiono Administer Procrit as orderedo Supplemental oxygen

Platelet <75,000

o Bleeding precautiono Monitor for abnormal bleedingo 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 Rhinitiso Prevention of anaphylaxiso Allergic conjunctivitiso Drug Allergieso Allergic dermatologic conditionso Blood Transfusion

First Generation Second GenerationBind to both central and peripheral H1 receptorsCauses drowsinessPossess anticholinergic effectsSome are used for motion sickness (30-60 min)

- Dipenhydramine- Promethazine

Bind to peripheral H1 receptorDoes not cross BBBNon-sedating

BrompheniramineDiphenhydramineChlorpheniramineDexchlorpheniramineCyproheptadineHydroxyzineClemastinePromethazineTripolidine

AzlastineCetirizineDesloratidineLoratadineFexofenadine

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 Bronchioleso Constricts Blood Vesselso Decreases capillary permeabilityo 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 pressureTo 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 thrombosiso 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, Cushing’s Syndrome, Ulcerogenic, Osteoporosis, Cataracts

o Immunosuppresants: may be used alone or in combination with corticosteroids Azathioprine (Imuran) Cyclophosphamide (Cytoxan) Cyclophosphamide (Sandimmune) Mycophenolate (CellCept)

Side Effectso Bone Marrow suppression

Anemia Administer Procrit as ordered

Risk for infection Risk for bleeding

*Avoid aspirin & NSAIDs

7. HIV:Opportunistic Infections

- PCPo 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 Inhibitorsi. Zidovudin AZT (Retrovir, Zidobudin)

ii. Didanosine (DDI) (Videx)iii. Zalcitabine (DDC) (Hivid)

2) Protease Inhibitorsa. Inhibit the viral proteases thus preventing viral maturation

i. Saquinavirii. Ritonavir

iii. Intinavir3) Entry/Fusion Inhibitors

a. Interfere with HIV CD4 receptor site binding and entry into cells i. Enfuvirtide (Fuzeon)

4) Nucleoside reverse transcriptase inhibitors- 1st druga. Zidovudin AZT (Retrovir) first drug approved for HIVb. Aslo used prophylactically for exposuresc. Must be taken q4-6 hours round the clock to keep increased blood

i. Adverse Effects1. Bone Marrow toxicity; drug resistance with long term use2. Nausea and HA most common SE3. Take ½ hour before or 1 hour after meals

HAART “Highly Active Anti-retrovial Therapy”- Combine 3-4 antiviral drugs

o Decreases chance of drug resistanceo Does NOT cure disease, can still transmito Many SE often want to stop medso 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 Marinolo 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 lighto Do not mix with other drugs in a syringeo IM or deep SQo 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 lighto Do not mix with other drugs in a syringeo Monitor for hypersensitivityo Interaction: Methotrexate, Phenytonin, contraceptiveso Teach to avoid alcohol and tobaccoo 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 SubQo Epogen Alfa (Procrit & Epogen)

Half-life: 4-13 hours peak within 24 hours (IV) peak 5-24 hourso Darbepoetin Alfa (Aranest)

Half-life is 49 hours-long termo 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 patient’s 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 fireo Unless life threatening bleeding is presento 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 reproductiono 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

o 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 can’t 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

o 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, Vinblastineo Structurally related compounds derived from the

periwinkle plant, Vinca rosea (vinca alkaloids) o Binds to the microtubular protein, tubulino 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” B-lymphocyte 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 TBo How will this kill tumor cells?

Immune system attacks cancer cells

*Know Chemo Man!!Cell Cycle Non-Specific Cell Cycle SpecificAlkylating AgentsAntibioticsCisplatinNitrosureas

- Effective for both low-growth fraction malignancies (Solid-tumors) as well as high growth fraction malignancies.

- Slow growing

AntimetabolitesBleomycin antibioticsVinca alkaloidsEtoposide

- Effective for high growth fraction malignancies (hematologic cancers)

- Rapidly growing

Disease Etiology/Risk Factors Assessment Symptoms Lab/Diagnostic Tests

Complications Medications/Treatment

Emphysema(COPD)Destruction of alveolar wallsDecreases surface area available for exchange. Increased resistance to pulmonary blood flowDifficulty in exhalation caused by airway obstructed by edema or excessive mucus production

- Lung hyperinflation due to air trapping

Increased work of breathing

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.

“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 positionCough mostly in AMPersistent tachycardia Dyspnea on exertion with advancing diseaseEnlarged accessory musclesClubbing of fingers (decreased oxygen) with disease progressionDiminished breath sounds & wheezing or crackles may be present on auscultation

Barrel ChestPursed lipsUnderweightTripod CoughTachycardiaDyspneaClubbing of fingers

ABG: slightly decreased PaO2. PCO2 is low during early stages of the disease (breathing faster-respiratory 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

Increased risk for pulmonary infection-Pneumonia

Can lead to pulmonary hypertension (more blood flow)

Cor pulmonale- right sided heart failure. Pumping makes right side bigger, works harder.

Dysrhythmias

Cancer

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 secretion-increased heart rate, constipation, nausea, urinary retention

- Atropine, ipatropium (Atrovent), Tiotropium Bromide (Spiriva)

Chronic Bronchitis(COPD)Disease of chronic airway inflammation & increase bronchial secretionCough lasting 3 months or more in 2 consecutive years Chronic inflammation of the airway causes hyperplasia of mucus glandsGoblet cells develop in abnormal sites in terminal bronchiolesCilia disappears and their clearance function is lost Mucosal edema and increased mucus progressively obstructs airway.

Inflammation, decreased cilia, increased mucus, can’t 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

TachycardiaTachypnea with use of accessory muscles Frequent pulmonary infectionFever in acute episode due to infection

CyanosisObesity- hypoxic-decreased activity, increased heart rate and respirationsCoughWheezing & RhonchiTachycardiaTachypnea 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 acidosisConstant Increased CO2 = decreased sensitivity (drive to breathe decreases), when O2 decreases = breathe

3) MethylxanthinesDirectly relaxes smooth muscles of the bronchial tree-bronchodilationAminophylline (Theophylline)

Anti-inflammation: 1) Steroids

Administer steroids to decrease inflammation within the airwaysIV: Hydrocortisone, methylprednisolonePO: Prednisolone, prednisoneInhalers: Beclomethasone, Triamcinolone, Fluticasone, Budenoside, Flunisolide inhalers

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 SOBExpiratory wheezesCoughFeeling of chest tightnessProlonged expirationTachypnea with use of accessory musclesTachycardiaDiminished or absent breath sounds (increased secretions)-maybe related to atelectasis or pneumothroaxExtreme restlessness, anxiety and agitationIntercostal retractionsUse of accessory musclesHyper-resonant sound on percussion

(airway decreased, increased secretions)

SOBWheezingCoughChest tightnessLong expirationTachypneaTachycardiaDiminished or absent breath soundsRestlessnessIntercostals retractionsHyper resonance

ABG: decreased PO2, mild respiratory alkalosis during initial attack, respiratory acidosis with disease progression

CBC: elevated Eosinophilscount 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 obstructionDone before and after use of aerosol bronchodilators to determine the reversibility of airway obstructionDecreased FEV or peak expiratory rate flow (PERF) during attack

Status Asthmaticus: severe, prolonged asthma attack which cannot be broken by usual treatmentWheezing may be absent

- Silent chestSevere acidosisMay have to intubate

Early: alkalosis, and good O2.Late: acidosis

2) Leukotriene Inhibitor/Modifiers

Suppress inflammatory process by blocking a group of inflammatory mediator called Leukotrienes

- Montelukast (Singulair), Zafirlukast (Accolate), Zileuton (Zyflo)

3) Mast Cell StabilizersMast 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-antitrypsintherapy for patients with deficiencyAdminister Antacids, H2 Blockers, or proton pump inhibitorAdminister diuretics if patient develops RHF

- Furosemide, Bumetanide

Administer Vaccines - Pneumonia - Flu- (may precipitate

asthma attack) 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 sat-check H&H too! Monitor sputum for color, amount, semi-fowlers. O2 @ 2L/min. Rest. Increase OFI 2000-2500ml & 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 patient’s decision, referral-counselors, 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 patient’s baseline. Green: 80-100%Yellow: 50-80%Red: 50% or less-need bronchodilator and medical treatment if yellow

Pleural Effusion

Accumulation of fluid in the pleural space

Disease/abnormality

Turning, Incentive S.

Transudate: Fluid contains some proteinFluid 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

EmpyemaPleural fluid containing pusAssociated with infectious process: pneumonia, tuberculosis, lung abscess

ChylothoraxDisruption of pulmonary lymph: surgery, traumaProduces fat malabsorptionfrom 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 accumulatesDiagnostic 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 position-opens 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

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/HemothoraxAir accumulation in the pleural spaceSpontaneous*

1) Simple or closed pneumothroax

Rupture of air bleb allows pathway of air movement between respiratory system and pleural spaceCollapse of involved lung tissue

NO OPENINGLung collapse from air bleb

Abrupt onsetPleuritic Chest PainDyspnea TachypneaDecreased Breath Soundson affected sideAssymmetrical chest movement

Spontaneous pneumothorax: in otherwise healthy client resolve without invasive treatment.

For recurrent spontaneous pneumothorax, pleurodesis may be indicated.

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

Hyperresonance on affected side because it is air filled

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

2) Tension pneumothoraxAir 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

Anxiety/RestlessnessSevere dyspneaAbsent breath sounds on affected sideTachypneaTachycardiaPoor colorAccessory muscles useJVDNarrowing pulse pressureHypotensionTracheal deviation (late)

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

3) Traumatic or OpenDisruption of the pleura, bronchi or lung tissue cause by blunt or penetrating trauma with air accumulation in pleural spaceOpening in chest cavity that allows air to enter pleural cavity. Causesthe lung to collapse due to increased pressure in pleural cavityCan be life threatening and can deteriorate quickly

DyspneaSudden sharp painSubcutaneous emphysemaAbsent lung sounds on affected sideRed bubbles on exhalation from wound Asymmetrical chest movementDecreased respiratory excursion

For OPEN pneumothorax, seal defect and secure only on 3 sides.

Placement of chest tube with water seal drainage.

Hemothroax

Occurs when the pleural space fills with blood. Usually occurs due to lacerated blood vessel in throax. As blood increases, it puts pressure on heart and other vessels in chest cavity. Each lung can hold 1.5 liters of blood

Anxiety/restlessnessSigns of shockFrothy bloody sputumAbsent breath sounds on affected sideCyanosisDullness on percussion of affected sideFlat neck veins (decreased blood)

CXR reveals pneumothorax or hemothorax ABG shows decreased PaO2.

Collaborative care: impaired gas exchange, ineffective breathing pattern, decreased cardiac output, pain, anxietyMonitor 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 Etiology/Risk Factors

Assessment Symptoms Lab/Diagnostic Tests

Complications/Additional information

Medications/Treatment

PneumoniaInflammation of lung parachyma7th 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.

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; inflammationInfectious debris and exudates fill alveloli; consolidation; impaired gas exchange

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 organismDetermine 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/brushingGet 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

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 collectedNursing 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 CiproNarrow spectrum after culture result is noted.

Bronchodilators: (if bronchoconstriction or spasm)

Sympathomimetics (bronchodilation)Albuterol/Proventil; Alupent

Methylxanthines (bronchodilation)Theophylline/Aminophylline

AntipyreticsTylenol 650 mg po q 4 for temp > 101

Liquefying Agents: Mucomyst, Guaifenesin

Complementary therapy: Echinacea- herb that stimulates immune function. – don’t take with autoimmune disorder. Will increase immunity.

1) Acute Bacterial Streptococcus Pneumoniae

Very sick episode with this type of pneumonia. Generally resolveswithout residual lung changes. Organism usually is Streptococcus Pneumoniae

Rapid onsetShaking chills, fever, coughRust colored or purulent sputumPleuritic chest pain (hurts to breathe in)Decreased breath sounds or crackles

2) Viral – “walking pneumonia”

10% of pneumoniasOrganisms= influenza & adenovirus

More mild than bacterialCommunity outbreaks generally viral.

HAFatigueMalaise

Organism multiplies outside alveoli in the alveolar septum & intestinal spaces of lungs

Dry coughMuscle aches

3) Fungal Histoplasmosis-histoplasma capsulatum(bird poop)

Amphotericin B-very potent-Often a serious acute reactionafter 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. *NephrotoxicItraconazole & Corticosteroids

4) Pneumocytis Carinii Pneumonia (PCP)

75-80% of those with AIDSdevelop (opportunistic) Also develops with immunosuppressive therapies

Fever of abrupt onsetTachypnea with SOBDry non-productive coughSignificant resp distress; requires ventilator

5) Aspiration Pneumonia

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

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 hand3) 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 ABG’s as ordered. Changes are early indicator of imp. Gas exchange. Want O2 > 80 mmHg and CO2 <45 mmHg. Fowler’s 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.



Complications/Additional Information


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

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

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 tissuearound 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

Reactivation TB:-occurs when a person’s 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

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.

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 non-communicable 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 Anti-tuberculosis 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. Chest Xray- for diagnosis

and evaluation.

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

***KNOW MED SLIDE ON PWRPT

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

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 patient’s room. Priority Nursing Diagnoses: ineffective breathing pattern, ineffective health maintenance, imbalanced nutrition: less than required, hyperthermia, pain, activity intolerance, isolationInterventions: 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.



Complications/Additional Information


Pulmonary Embolism Clots: typically caused by 3 factors: hypercoagulablestate, vessel trauma, venous stasis-Manifestations will depend upon where the thrombus occurs and/or where the emboli becomes trapped in the vasculature.

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

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

ABG: hypoxemia (PaO2 <80). Hypocapnia and respiratory alkalosis acidosisColor-flow Doppler Imaging: for DVTs (if positive start anticoagulation)Pulmonary angiography:contrast medium injected into the pulmonary arterySpiral CT: it visualizes main, lobar & segmental pulmonary emboliFDP (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 FDPV/Q scan: radiogatedalbumin 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.

Coagulation Studies: PTT: intrinsic clotting pathway-Heparin- 1.5-2 times the controlled value.PT/INR: extrinsic clotting pathway-Warfarin- 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 36-72 hours. 5-7 days to be fully effective. The recommended therapeutic range for venous thromboembolism is an INR of 2-3. Once the patient isstabilized on a specific dose, the INR may be checked every 1-2 weeks. –don’t 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 HEARTAntilipidemic 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

1. Statins Mode of Action:

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

Examples: Mevacor (Lovastatin) Prevachol (Pravastatin) Zocor (Simvastatin) Lipitor (Atorvastatin) Lescol (Flovastatin)

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

2. 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

Hepatotoxic Monitor LFT

Can potentially increase blood sugar

3. 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-α (PPAR- α)

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


Assessment Symptoms Labs/Diagnostic Tests

Complications/Other Information


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.

Occurs over timeCAD 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 replacement-birth control pills especially problem for women who smoke. Hyperlipidemia-LDLs promote cholesterol deposits on arterial walls. VLDLs: cary triglyceride HDLs: clear cholesterolfrom arteries, take back to liver for excretion; increase with exercise, weight loss, smoking cessation. hypertension, diabetes mellitus

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 40-150 mg/dL (desire <150). NPO for 12 hours (after dinner).

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”

1) Stable: Increased demand, decreased supply of oxygen. Rest-relieved. *Nitroglycerin.

2) UnstableBlood 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 after-load. Non-dihydropyridines also lower heart rate and decrease contractility. Dihydropyridinesmay aggravate angina in some patients due to reflex tachycardia.

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. Cresendo-decresendo 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. Transesophagealechocardiography (TEE) How much blood with contraction. NPO-check gag reflex. Ejection fraction-more sensitive-ischemia 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, tachycardia-beta blockers to decrease, severe throbbing headache-dilation 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 hoursovernight. 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. 70-75% 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 Etiology/Risk Factors Assessment Symptoms Labs/Diagnostic Tests


Medications/ Treatment

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

White Blood Cells & ESR: inflammation, myoglobin increased in bloodstream. ECG changes

**Understand Cardiac Serum Markers Chart!

Circulation: Percutaneous Transluminal Coronary Angioplasty with or without stent (PTCA). Or Percutanous Coronary Intervention (PCI)Nursing care similar to cardiac angiograpyCABG: 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 airwayBreathing: 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 returnThromolytic Therapy: within 3-12 hours: altepase, streptokinase, reteplase, anistreplase. Heparin drip post thrombolytic agent. Administer anti-arrhythmicsif 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.


Assessment Symptoms Labs/Diagnostic Tests



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.

(legs down)Acute painIntermittent claudicationColdnessWeak pulsesParasthesiaPallor when limb is elevated.Rubor when limb is dependent (down)Hair loss distant with occlusionThick brittle nailsNo edema: but ulcers in distal areas, foot, toes, ankles and calves.

Intermittent claudication (stable angina of legs) Food or toe wounds that won’t heal or heal very slowly.Gangrene (dry) A marked decrease in the temperature of your lower leg or footWeak peripheral pulses

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 non-invasive 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.

Stop smoking, avoid becoming chilled, wear warm socks, boots, gloves, warm water baths. Exercising to stimulate circulation-as long as it doesn’t cause pain. Don’t keep legs elevated. Antilipidemic Drugs. Anticoagulants & Antiplatelets, Vasodilators, Manage stress

Peripheral Artery Angioplasty: for patients that conservative treatments aren’t enough.

Peripheral Bypass Surgery: if there’s a long portion of artery in your leg that ‘s completely blocked and you’re having severe symptoms, surgery may be necessary.

1) Thromboangiitis Obliterans (Buerger’s Disease)

clot inflammation of vessel that blocks and kills tissue.

Acute arterial occlusion. Inflammatory vasculitis causing the thrombus formation. Distal arterial ischemia.

Non-modifiable: being a man, over 50, asian

Modifiable: smoking (vasoconstriction, inflammation), obesity, hypertension, high cholesterol.

2) Reynaud’s Disease

Periodic constriction of arteries that supply extremities, mostly hands and feet.

Frequently seen in young women.

Signs and symptoms usually precipitated by exposure to cold, emotional upset and tobacco usage.

Pain: client learns warmth relieves pain. Relieves vasospasms, blood rushes to the extremity. NumbnessColdnessTingling lasts minutes-hours.

Venous Disorders (Peripheral Venous Disease)

Little or no pain, some tenderness along inflamed vein. Warm skin temperatureCyanotic if dependent positionEdema typically presentPulses normal and

presentThrombophlebitis/Venous Thrombosis (clot-inflammation)

Formation of a thrombus in association with inflammation of vein. Classified as either superficial or deep. 65% of IV therapy-superficial5% 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 Homan’s sign: pain upon dorsiflexion of foot. Not always present in all cases.

Lungs make heparin, compartment syndrome.

Virchow’s 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

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 heparinfor those at risk (surgery, bedrest)Early mobilizationLeg 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 heartTEDS or pneumatic compression devices to legs.

Treatment: bed rest with leg elevated until tenderness is reduced. Don’t massage legs, no SCD, no leg exercises. Anti-coagulants like Heparin drip for acute treatmentWarfarin, 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.

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

Causes: atherosclerosis (primary reason) Hypertension (contributing factor)

Location: Thoracic, abdominal, cerebral. Typically in the aorta.

70 year old maleSmokerHigh blood pressureCABGCholecystectomy Inguinal Hernia RepairAAA

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 weekThen oral anticoagulants or ASAoften 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

3) Aortic Dissection

Tear in the intima of the aorta, blood forced between layers of aorta. Creates blood-filled cavity that can expand length of aorta.

Primary sign: sudden excruciating pain (ripping or tearing sensation)

- Abd aorta = abdominal pain

- Thoracic aorta = chest or back pain

Distal pulse absent as dissection further occludes blood flow. Paralysis eventually possible (decreased blood flow to spinal cord)

Treatment

Nursing Responsibilities: Pre-op: may do brief teaching if emergency. Deal with client’s 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.

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 HypertensionPrimary HTN

- 90-95% of cases - Also termed “essential” of “idiopathic”- NO known cause but risk factors include:

Family historyIncreased Na IntakeObesityInactivityExcessive Alcohol intakeSecondary HTN

About 5% of cases Renal or renovascular disease Endocrine disease

PheochomocytomaCusing’s syndromeConn’s syndrome

Primary HTN Risk FactorsNon-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 resistanceModifiable

Diet High Na Intake

ObesityExcess alcohol consumption

Alcohol causes vasoconstrictionStress

High level of catecholaminesSmoking

Causes vasoconstriction Complications of DiabetesMyocardial Infarction & heart failureRenal Failure

StrokeRetinopathy

Assessment:Subjective

Family history of HTN or CVDReports of fatigue, blurred vision, & headacheReports 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 & triglycerideElevated BUN & CreatenineAbnormal UrinalysisCardiomegaly on CXRAbnormal ECG

Nursing DiagnosisDecreased cardiac outputIneffective Health MaintenanceRisk for non-compliancePlanning and ImplementationInform 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 pressureAerobic 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 ImplementationAlcohol 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 ImplementationSmoking 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

MedicationsDiuretics- prompt kidneys to excrete sodium, which reduces blood volume and thus blood pressureAdrenergic 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 outflowCalcium Channel Blockers - prevents calcium from enabling muscles cells to constrict around the blood vessels, thus dilating the vesselsACE inhibitors - Dilates blood vessels by blocking enzymes which cause artery walls to constrict

DIURETICSDrugs that can Decrease PreloadPurpose 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: Decreased preload Decreased cardiac output

Overall effect: Decreased workload of the heart Decreased blood pressure

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)

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 lbsTeach how to prevent orthostatic hypotensionAvoid 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 diureticsMay 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 ¼ of the normal dose Teach prevention of orthostatis and monitor BP regularly

Adrenergic Blocking AgentsBeta-blockersAct in the periphery by blocking beta receptors

2 types: Cardioselective primarily affecting β1 Non-cardioselective affecting both β1 & β2

Reduce heart rate due to beta1-blockadeBronchoconstriction due to Beta2-blockade

All the names of β-blockers ends in “lol” Examples:

Propranolol (Inderal), Atenolol (Tenormin). Metropolol (Lopressor), Nadolol (Corgard)Adrenergic Blocking AgentsSide effects

ImpotenceBradycardiaFatigue

Mask symptoms of hypoglycemiaBronchoconstriction CI to asthmatic patientsArrhythmia 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 ClonidineMethydopa

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 EffectsDry mouthSedationImpotenceConstipationRebound hypertension when stopped abruptlyDepression

Nursing ImplicationsTeach 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 RAASAngiotensin-converting enzyme inhibitors

Angiotensin II receptor blockersDecreases 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 EffectsFatigueDizzinessHeadacheFetal InjuryHyperkalemia Renal failure – Monitor BUN & CreateninNeutropenia – Monitor WBCDry, nonproductive cough, which reverses when therapy is stopped (Due to Bradykinins)Angioedema (Bradykinins)NOTE: First-dose hypotensive effect may occur!Nursing ResponsibilitiesMonitor VS and compare with baselineMonitor potassium levelKnow BUN and Createnine before beginning treatmentHold and inform MD if BUN and Createnine increasesTeach prevention of orthostasis Not for pregnant womenAspirin and NSAID can decrease the efficacy of ACE inhibitorsTeach patient that Dry cough is common adverse effectMonitor 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 EffectsHeadacheMay cause occasional dizziness, inability to sleep, diarrhea, dyspnea, heartburn, nasal congestion, back pain, fatigueHyperkalemia Fetal harmRenal failureNursing ResponsibilitiesMonitor VS and compare with baselineMonitor potassium levelKnow BUN and Createnine before beginning treatmentHold and inform MD if BUN and Createnine increasesTeach prevention of orthostasisMaybe taken with or without mealNot for pregnant womenAspirin and NSAID can decrease the efficacy of ARBsFluconazole may increase antihypertensive effectsRifampin may decrease antihypertensive effect

CALCIUM CHANNEL BLOCKERSDecreases 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 EffectsHypotensionFlushingConstipationDizzinessHeadacheReflex 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 EffectsCardiovascular

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

VASODILATORSMechanism 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 BlockersBeta BlockersCa Channel BlockersACE InhibitorsNitrates

-lol -pril -pine-nitr -zosin

Drugs for Heart FailureCauses

◦ 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 distentionHepatomegalyPeripheral edemaSacral edemaLeft sided failure

Pink Frothy SputumDyspnea CyanosisSOBCrackles at base of lungsOrthopnea FatiguePND

Compensatory MechanismsWith failure there is drop in COEntire body receives less bloodBody thinks Blood Volume has dropped

Compensatory mechanisms begin:◦ SNS Stimulation◦ RAAS◦ Cardiac Remodeling◦ Release of ANP & BNP◦ Heart Failure

Compensatory MechanismsSympathetic 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 FailureKey Investigations

12 lead ECG, Chest X-Ray, Blood gasesU&E’s

◦ 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

VasodilatorsArterial 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 retentionAssess resp (declining resp status, indicator of worsening left heart failureNotify 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, doesn’t 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, Paget’s 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 sprayo It inhibits osteoclast activity, decreases bone resorption thus lowers serum calcium and

phosphate and reduces bone pain, it increases BMD in the spine. Paget’s 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) & D-

penicillamine (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 acido Allopurinol

Uricosuric drugs- inhibits tubular absorptiono Probenecid or Sulfinpyrazone

Knee & Hip Replacements: pre-antibiotics, enoxaparin (lovenox), fondaparinux (arixtra), Coumadin (Warfarin)

Alzheimer’s 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 Alzheimer’s 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 can’t get back in, suppresses anti-inflammatory 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

test prior to each dose. Determine LVEF: prior to 1st 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), DantroleneOptic Neuritis-Methylprednisolone, Oral steroidsFatigue-antidepressant, amantadinePain-Codeine, AspirinSexual dysfunction-ViagraTremor-Primidone, Propanolol

Parkinson’s Disease2 major categories:

1) Dopaminergic agents a. By far the most commonly used for PD. Promotes activation of dopamine receptorsb. 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 shouldn’t 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 amphetamineAmantadine (Apokyn): promotes dopamine release. These drugs stimulate the actions of dopamine in the brain, reducing the symptoms of Parkinson’s 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.

- 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 agentsa. 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 ClosedCompleteIncomplete

Types of Fracture Based on Mechanism of Injury- look at picture*- Normal, transverse, oblique, spiral, comminuted, segmental, avulsed, impacted, torus, greenstick

Fractures Healing1) Neonatal period

o 2-4 weeks2) Early childhood

o 4 weeks3) Later childhood

o 6-8 weeks4) Adolescence

o 8-12 weeks

Assessment – look at table*Monitor for complications:

- Compartment syndromeo Result from increase pressure in the tissue compartment leading to decreased perfusion to tissues and

nerveso The five Ps: Pain, Pallor, Paresthesias, Pulses, Paralysiso Volkmann’s ischemic contracture

Result from unresolved compartment syndrome Ischemia causes degeneration and contracture of muscles

- Fat Embolism Syndromeo Fat globule lodge in the pulmonary vasculature or peripheral circulation o Common in long bone fractures and major traumao During first 12-72 hours post injuryo 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 Thrombosiso Virchow’s Triad: Blood, Vessel, Flow

Hypercoagulability, venous stasis, turbulent blood flow- Infection

o Likely to occur in open fractureo May result from contamination at the time of injury or during surgeryo Can result into delay healing and osteomyelitiso WOF: wound drainage, fever, pain, odor

Collaborative CareTherapeutic 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 integrityDiagnostic 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 Reduction1) Closed Reduction (conservative)

o For simple fractureso Bring the bone together by manipulationo Cast, Splint or Tractiono X-ray post reduction

2) Open Reduction Internal Fixation (ORIF) (operative) o For complex fractureso Surgery o Reduction is achieved by through internal fixation

3) Mixedo 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) Tractiono Traction is exerting its grabbing or pulling force through the client’s skin.o Short term treatment 24 – 48 hourso 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 Tractiono Several forces work in unison to raise and support the client’s 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-tractiono Pulling force exerted in a opposite direction to prevent the client from sliding to the end of the bedo Client’s weighto Elevating foot of bedo 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 client’s 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 dryo Fiber glass will take 1 hour to dry

Nursing Responsibilities for Patients with CastFrequent 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 & CastPin-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

o 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 FracturesTypes: 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 posteriorlyAtypical Symptoms

- Vague pain: Buttocks, Knees, Groin, Thigh- Ability to walk is unaffected

Interdisciplinary CareDiagnostics: X-Ray, MRI & Bone scanTreatment: 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 AmputationGuillotine

- When there is infectionClosed

- 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 conditiono Teach to do active ROM on other extremities

- Prevent edemao Avoid dangling stump over bedo Elevate limb for the 1st 24 hours

- Prevention of hip contractures o Lay prone for 30 minutes 3-4 time a dayo Avoid elevating or sitting with residual limb on pillows to prevent flexion contractures

- Prevent external rotation and abduction contractureso Correct alignment in bedo Place rolled towels or sand bags when in chair prevent external rotation

- Assess types of dressingso Application of prosthesis immediatelyo Cast/rigid dressingo Elastic wrap dressingo ACE bandage for conical shape & decrease edema; wrap distal to proximalo 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-opProsthetics

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: Anti-seizure & 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 laterFracture1.5 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 stresso Height loss, Kyphosis, Low back pain: As vertebra collapse it puts pressure on nerves causing pain that

radiates to flank and abdomenBone 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, & Paget’s 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 Dual–energy 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 activityo Reflects bone turn over

- PTHo Maybe high or normal

- Urineo 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 supplementso Calcium carbonate

Generic = 200-600mg Caltrate = 600mg TUMS Ultra = 400mg

o Calcium Gluconate – provide lower amount of elemental calcium that carbonateo 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 800Up to age 24 1200-1500Pregnant & breast feeding 1200-1500Women 25 –50 (premenopausal) 1000Women over 50 (Postmenopausal)Taking ERT 1000Not taking ERT 1500Men 25 to 65 1000Men 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 50Mechanism:

- Decreases osteoclastic activity & increase osteoblastic activityDose:

- 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 HDLDisadvantages

- 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 qdAdvantages

- Increases bone density, Decreases fracture risk, No stimulation of breast or endometrial tissue, Decrease LDLDisadvantages

- Increased risk of DVT, Not for women with history of blood clots, Doesn’t treat post-menopausal symptoms, May increase hot flashes, No effect on HDL

BisphosphonatesApproved 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, Paget’s 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 dosingDisadvantages

- 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 spineIndications: Paget’s disease of bone, Osteoporosis, HypercalcemiaSide 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 toesRisk 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 gratingor 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. Bouchard’s 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 careTherapeutic 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 symmetricalAs disease progresses characteristic deformities appearLabs

- 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 painTeach how to use assistive devices

- Pharmacologic Managemento 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 crystalso 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 CareTherapeutic RegimenGoalTerminate acute attacks Control of pain and inflammation Prevent future attacks Reduce serum uric acid levelsPharmacotherapyNSAIDCorticosteroidCholchicine

AllopurinolJoint replacementArthroplasty

Nursing DiagnosisPainImpaired physical mobilityIneffective health maintenancePlanning and ImplementationTeach Dietary modificationLow fat & low cholesterol dietFasting is contraindicated – WHY?Increase fluid intake (3 liters per day) when taking medicationsAvoid foods that are high in purineTurkey, organ meat, sardines, smelts, mackerel, anchovies, herring , bacon, beans, lentils, spinach, asparagus, mushrooms, cauliflower, oatmeal, ETOH, legumesTeach to avoid of AlcoholConsumption can increase uric acid production. Inhibits uric acid excretion in the kidney

Pharmacotherapy ColchicineAnti-inflammatory effects limited to goutInhibits crystal-induced production of chemotatic factorsSide Effects PO - Abdominal cramping, diarrhea, nausea, vomitingIV - Local pain, DIC, tissue damage on extravasationContraindications - Significant GI, renal, hepatic or cardiac diseaseQuestionA 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 drugsGoal is for serum urate concentration to be at 6mg/dL or lessXanthine oxidase inhibitorsAllopurinol (Zyloprim): blocks conversion of xanthine to uric acid. Start at lower doses with renal impaired patientsUricosuric drugsProbenecid or Sulfinpyrazone: increase renal clearance of uric acid by inhibiting tubular absorptionSide effects may prohibit use - GI and kidney stones

Pharmacotherapy

Avoid use of medications that contribute to hyperuricemia: Thiazide and loop diureticsLow-dose salicylateNiacinCyclosporineEthambutol

Definition Assessment/Risk Factors Symptoms Lab Tests Management MedicationsHyperparathyroidism

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 injuryPainImpaired physical mobilityRisk for altered urinary eliminationRisk for constipationKnowledge deficit

*2x more common in women

-Health history-Vital signs-EKG-Elimination pattern-Nutrition status-Activity intolerance-Cognitive-perceptual and sensory function-Neuromuscular function

-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

Elevated total serum calcium. Normal values 9-11 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

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 osteoporosisStrain urine-risk for stonesIncrease OFI 2000-3000 ml/dayIncrease fiber in diet (constipation)Encourage activity as tolerated, pace activity with rest periodPromote nutrition, and fluid and electrolyte balanceWeigh dailyPrevent 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

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 Assessment/Risk Factors Symptoms Lab Tests Management MedicationsHypoparathyroidism

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 intakeDeficient knowledge: disease process and drug therapyRisk for injury: tetany, sedation, seizuresRisk for injury: hypercalcemia/hypocalcaemia

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!

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. Chvostek’s sign/Trousseau’s sign, seizure, coma, death

Dry, thin, hair, alopecia areata, ridged finger nails

Decreased PTHIncreased Serum Phosphate

Increase serum calcium levelNutrition consultSupplemental calcium and vitamin DHigh calcium diet Calcium gluconate

Planning/Implementation:Medic Alert braceletPromote comfort and restPrevent falls, may need walkerTeach about signs of tetanyEncourage activity as toleratedPace activity with rest periodPromote nutrition and fluid and electrolyte balanceTeach about foods high in vitamin DTeach about foods high in calcium: cheese, milk, turnip greens, almonds, beans, frankfurters, and bologna. *Don’t take turns several times a day-impairs absorption and won’t absorb well.

Goal is to increase serum calcium level. Must have calcium gluconate at bedside. Nutrition consult. Supplemental calcium/Vitamin D.

Restore calcium balance-high calcium diet.-no more than 2500 mg/day.

10% calcium gluconate 10-20 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 hormonesThe 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 Assessment/Risk Factors Symptoms Labs Management MedicationsHyperpituitarism(Anterior) Characterized by increased production of one or more tropic hormones. Most common caused by benign adenoma.

Visual changesIncreased Growth hormone, Prolactin, ACTH or TSH

-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

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

1)Gigantism/Acromegaly (Excessive GH)

Ocreotide (Sandostatin)-GI side effects, Expensive

2) Cushing’s Disease(Increased ACTH-increased cortisol)3) Secondary Hyperthyroidism(Increased TSH)-increased metabolic rate4) HyperprolactinemiaFemale: decreased libido, irregular or absent menses, difficulty becoming pregnant

Male: Decreased libido, gynecomastia, galactorrhea, impotence

Definition Assessment/Risk Factors Symptoms Lab Tests Management MedicationsHypofunction of the Anterior Pituitary Gland

-Panhypopituitarism-Sheehan’s syndrome (autoimmune)

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

Hormone replacement

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 tumors-carcinoma of the lungs, leukemia, pancreatic cancer, Hodgkin’s diseaseDiureticsBarbituratesAnesthetics

Nursing Diagnosis:Altered thought processAcute painImbalance nutrition less than body requirementsFatigueDeficient knowledge

Characterized by high levels of ADH in the absence of serum hypo-osmolality

Water intoxicationCellular edemaDilutional 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

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 recommendedIf 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: Implement fluid restriction to prevent further hemodilution.-frequent oral hygiene, ice chips or sugarless chewing gum can decrease thirst

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. Neuroassessment. Elevate HOB to not more than 10 degrees-fool 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 Assessment/Risk Factors Symptoms Lab tests Management MedicationsDiabetes 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

-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

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 ADHRisk for impaired skin integrityRisk for injury r/t electrolyte imbalanceRisk for constipation Dehydration

Urine specific gravity <1.005Urine osmolality <300 mOsm/kgSerum 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 DIBefore 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 hourThe 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

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 treatmentof 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 sugar-hyperglycemia 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

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 Assessment/Risk Factors Symptoms Lab Tests Management MedicationsHyperthyroidism

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 (Grave’s 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 outputDisturbed sensory perception (visual)-exothalamusRisk for ineffective airway clearance –GoiterHyperthermia-heat intolerance-activity intolerance – HR, decreased CO, increased BMR-Risk for imbalanced nutrition less than body requirements: increased BMR

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.

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 administrationSymptoms of hyper and hypoInstruct to report signs of hemorrhage, hypocalcaemia, respiratory difficulty, incisional infection Support neck to avoid strainWound careLimit coughing and strain talking-regular eye exam*Report changes in vision or appearance of eyesEye pain, closure of eyelidsEye exudates, photophobia*Sleep with HOB elevated -protect eyes-artificial tears, eye patches

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 Lugol’s 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.

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 comfort-analgesics, semi-fowler’s 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.)

Ethionamide Drugs for lifeAblative radioactive I-131Thyroidectomy Partial or Radical-shrink thyroid before surgery to decrease risk of thyroid storm. *Increased calorie, increased protein diet, dairy products-on 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 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)

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.

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 (Hashimoto’s 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 outputHypothermiaConstipationRisk for skin integrity impairmentRisk for activity intoleranceRisk for sexual dysfunctionDisturbed body image

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

***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 it’s increased,secondary it’s 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 awayTriidothyronine (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 Assessment/Risk Factors Symptoms Lab Tests Management MedicationsCushing 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 tumorsSECONDARY-Cushing’s disease (ACTH-secreting pituitary tumor) Ectopic ACTH production in tumorsIATROGENIC- administration of exogenous corticosteroids *Increase in ACTH tells adrenals to release too much cortisol.

Nursing Diagnosis:Fluid volume excess-aldosterone, increased Blood sugarRisk for injury-osteoporosis, fracturesRisk for infection-bone marrow suppressionDisturbed Body Image-increased central weight, muscle wastingKnowledge deficit

Vital signs- decrease pulse and BPActivity intoleranceSkin condition-thin, bruise easyElimination pattern-constipationNutrition problemFluid and ElectrolytesSelf concept-look will change-retain water. Limbs are skinny, trunk edema Frequency of blood sugar monitoring-cortisol causes elevated blood sugar.

Elevated Serum CortisolElevated urine 17-KetosteroidsPlasma ACTH may be low, normal, or elevated depending on problem.

Cushing’s Syndrome:decreased or normal ACTH, increased cortisol. (negative feedback)

Cushing’s Disease: Increased ACTH, increased cortisol (pituitary’s fault)

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 cortisol-induced 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

ACTH suppression test:Cortisol and ACTH level should decrease in response to administration of dexamethasone.-if it goes down, it’s 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

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, non-skid 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.

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 Assessment/Risk Factors Symptoms Lab Tests Management MedicationsAddison’s Disease

From treatment of Cushing’s normally.

Insufficient level of cortisol because of destruction of the adrenal cortex. -autoimmune, TB, infarction, fungal infection, AIDS, Metastatic cancer, Iatrogenic Addison’s disease may be due to adrenal hemorrhage.

More common in women <60 years old.

*Decreased cortisol and aldosterone

Nursing Diagnosis:Deficient fluid volumeRisk of ineffective therapeutic managementRisk for electrolyte imbalanceDeficient knowledge

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

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

Subnormal levels of cortisolDecreased 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 (Addison’s 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

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

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 middle-aged 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.

Severe episodic hypertensionSevere pounding headacheTachycardia with palpitationsProfuse sweatingAbdominal or chest pain

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 Assessment/Risk Factors Symptoms Lab Tests Management MedicationsDiabetes 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

*Understand 2 charts in the PowerPoint

**Know oral agents for insulin in the PowerPoint.

Sulfonylureas Meglitinide analogsInsulin Sensitizers-Biguanides -Thiazolidinediones or Glitazones A-Glucosidase Inhibitors-Acarbose and Miglitol Amylin and IncretinDipeptidyl Peptidase-IV inhibitors Synthetic Amylin Analog

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

Normal Blood Glucose = 70-110 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 = <7-9%. 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

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.

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 insulincan be given IV. DKA –Hyperkalemia.

Ultra fast/ultra short acting: lispro (Humalog), aspart (novalog), glulisine (Apidra)Short acting: regularIntermediate: NPHUltra long acting: glargine (Lantus) /detemir (Levimir)*Know chart & length of time

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