Bad Bad Drugs

Bad Bad Drugs: Drugs we love to make errors with:

Margi says these will show up on the final exam. Just because they are bad bad.

Heparin: comes in 1000, 5000, 100, 10000 units/ml.

Insulin: Several kinds and several patients on insulin. We need to know forever the onset, peak, and duration of the different insulins. It’s actually hard to kill people with insulin, but you can certainly harm people.

Morphine Sulfate: IV, PO, IM, SubQ.

KCl: this is a good way to kill people.

Coumadin: fussy and amplified with other protein bound drugs. Always always check PT/INR.

Nursing students make the most errors with Insulin.

Anti Inflammatory and Anti Infective Agents

N203 ANTI-INFLAMMATORY AND ANTI-INFECTIVE

AGENTS

Objectives: Upon completion of this class, the student will be able to:

1. identify the five cardinal signs of inflammation;

2. describe the action, indication for use, and potential adverse effects of aspirin

and ibuprofen NSAIDs;

3. describe Gold as the prototype for anti-arthritis;

4. describe allopurinol as the prototype for antigout;

5. explain the mechanisms of action, general adverse effects of antibacterial

drugs;

6. describe the prototypes of each type of antibacterial agents;

7. describe the prototypes of antitubercular drugs, antifungal drugs, and

metronidazole;

8. describe the prototypes of antiviral drugs and urinary antiinfectives;

9. discuss the nursing process with safe administration of these agents.

I. INFLAMMATION

A. Characteristics: cardinal signs; what are they?

B. How can it be prevented?

Inflammation: [heat, redness, swelling, edema, pain, all lead to ‘loss of function’]. Response to tissue injury. Lead to removal of dead cells. Want to stop it when: inappropriate inflammation or chronic painful inflammation. Always means you’re suppressing the immune system: risk for infection.

Tissue damage: arachadonic acid is released from tissue cells, that wakes up the prostaglandins and leukotrienes, and those stimulate nociceptors.

II. ANTIINFLAMMATORY AGENTS

A. How do they work?

B. Prototype: Aspirin:

action: analgesic, antipyretic, prevention of platelet aggregation, and anti-inflammatory by inhibiting prostaglandin synthesis, inhibiting hypothalamic heat-regulating center

caution with renal or hepatic disorders

adverse reactions: tinnitus, ulceration, agranulocytosis, bronchospasm,

thrombocytopenia;

C. Nonnonarcotic Analgesics: NSAIDs: non-steroidal antiinflamatory drugs are things like OTC pain killers: Ibuprofen, naproxen, etc. Good for dull throbbing pain like inflam, headaches, cramps. Act on PNS at pain receptor sites.

NSAIDS: irritate GI, take on full stomach. Reduce inflammation

COX 1&2 inhibitors:

COX-2 inhibitors: “Cyclooxidase-2”. These block the 2 and not the 1—which means less GI upset and GI bleeding.

Ketoralac: [Toradol]

Non-steroid, but severe renal and hepatic impact; should only be used short term. This is about 5x as strong as morphine—it inhibits prostaglandins.

Action: It inhibits synthesis of prostaglandins by inhibiting both COX-1 and COX-2 enzymes. Is a peripherally acting analgesic.

Use: Exhibits analgesic, antiinflammatory, and antipyretic activity. Effective in controlling acute post-operative pain, Short-term management of pain;

Adverse: hemorrhage

Prototype: Celebrex (Celecoxib)

Use; analgesic, nsaid; cyclooxygenase-2 (cox-2 but not cox-1) inhibitor; antiinflammatory;

Action: Although an NSAID, unlike ibuprofen celecoxib inhibits prostaglandin synthesis by inhibiting cyclooxygenase-2 (COX-2)

Adverse: Increased risk of cardiovascular events.

2. Ibuprofen (Motrin)

Class: nsaid, cox-1 and cox-2 inhibitor; analgesic, antipyretic

Action: reduce inflammation and fever by inhibiting prostaglandin synthesis

Caution with bleeding disorders, early pregnancy, SLE

Adverse reactions: GI bleeding, blood dyscrasias, cardiac dysrhythmias,

nephrotoxicity

III. ANTIRHEUMATIC DRUGS

A. NSAIDs

B. Immunosuppressive agents

C. Immunomodulators

D. Chrysotherapy (heavy metal therapy)

2. No longer a prototype: Auranofin (Ridaura)

1. use/action: symptom relief, prevent deformities, depresses migration of

leukocytes, suppresses prostaglandin activity

Contraindication: patients with colitis, SLE, hemorrhagic conditions, renal or

hepatic disorders, HTN, CHF, DM, pregnancy

Adverse reactions: nephrotoxicity, hematuria, thrombocytopenia

IV. ANTIGOUT DRUG

Anti-Gout Drugs: gout is uric acid in the joints that causes burning sensation.

A. Prototype: allopurinol (Zyloprim)

1. action: reduces uric acid synthesis

Use: Antigout

2. caution with renal and hepatic disease

3. adverse effects: retinopathy, cataracts, bone marrow disorders

IV. ANTIBACTERIAL DRUGS

A. Mode of action

Either bacteriostatic [prevent multiplication] or bacteriocidal [destroy pathogenic cells]

1. inhibit bacterial cell wall synthesis

2. alter membrane permeability

3. inhibit protein synthesis

4. inhibit synthesis of bacterial RNA and DNA

5. interfere with metabolism within bacterial cell

Modes of action: need to know in general how these drugs work. Some are both types, depending on the dose.

B. Body defenses

1. nutrition

2. age

3. immunoglobulins

4. WBCs

5. organ function

6. circulation

C. Resistance to antibacterials

1. MRSA

2. VRE

D. General adverse reactions to antibacterials

1. allergic reactions

2. superinfections: esp fungal, and superinfections are likely when someone has been on antibiotics for more than 1 week.

3. organ toxicity

4. The worst adverse reaction: anaphylactic shock. Lots of people are allergic to penicillin, and that means they are likely to be allergic to cephalosporins. A lot of people are also allergic to sulphanomides.

5. Also heavy renal and hepatic impacts with these.

E. Nursing Responsibilities

Patients w/ infections: maintain skin integrity—when skin breakdown occurs, it is harder to repair in patients with infections.

We don’t culture people’s pneumonia too often any more: RBP says if someone got their illness in the community, it’s probably a gram positive, so we treat them one way until we get back a culture that says to switch meds.

V. PENICILLINS AND CEPHALOSPORINS

Penicillin has been around forever. Unfortunately they’ve been overused.

A. PCN prototype: amoxicillin (Amoxil)

1. contraindication: PCN allergy

Use: Good for both gram negative and gram positive infections. Who gets it: kids with ear infections, UTI’s, etc.

2. action: inhibits enzyme in cell wall synthesis, bactericidal

3. adverse reaction: superinfections, blood dyscrasias, respiratory distress

B. Cephalosporins

1. 1-4 generations: stronger and broader

2. prototype: cezazolin (Ancef), 1st generation

Use: Preop prophylaxis, UTI, bone, joint, soft tissue infections, bacteremia.

Action: Inhibits cell wall synthesis, destroys cell

caution: renal disease and PCN allergy

adverse reactions: superinfections, seizures, anaphylaxis

We prefer to use our ‘little guns’; our 1^st generation antibiotics, before we use our 4^th generation antibiotics.

VI. MACROLIDES, TETRACYCLINES, AMINOGLYCOSIDES,

FLUOROQUINOLONES

A. Macrolides: azithromycin (Zithromax)

1. indication for use: gm-positive and some gm-negative, with clients allergic to

PCN, respiratory infections, gonorrhea

2. action: inhibits steps of protein synthesis, bactiostatic or cidal

3. adverse reaction: superinfections, hepatoxicity

B. Tetracycline: Tetracyclines: Vibramycin: can have more adverse effects. Given when you need to step up the antibiotics b/c you have an uncommon bacteria or unresponsive strain.

Doxycycline (Vibramycin)

1. caution: with alcoholism, hypokalemia, bradycardia

2. action: inhibits steps of protein synthesis, cidal or static

3. use: treat infections by uncommon bacteria

4. adverse: blood dyscrasias, hepatoxicity, CNS toxicity

C. Aminoglycosides: Aminoglycosides: these are super nephrotoxic. Gentamycin. They are for super sepsis situations. There are protocols to check BUN and Creatinine, etc, the pharmacy manages it based on body weight, etc.

Gentamicin (Garamycin)

1. action: inhibits bacterial synthesis, cidal effect

2. use: serious infections from gram-negative bacteria, PID, MRSA

3. adverse: oliguria, superinfection, ototoxicty, nephrotoxicity, liver damage

D. Fluoroquinolones: Levofloxacin (Levaquin)

1. action: interferes with DNA enzyme, cidal effect

2. use: lower respiratory tract, renal, bone, joint infections

3. adverse: encephalopathy, seizures, dysrhythmias

VII. SULFONAMIDES: may potentiate sulfonylurea-induced hypoglycemia

Co-trimoxazole/tmp-smz (Bactrim): combination of sulfamethoxazole (SMZ), a sulfonamide, and trimethoprim (TMP)

A. action: inhibits protein synthesis, cidal effect

B. use: complex UTI, bronchitis, PCP [Pneumocystis carinii pneumonitis most common death in AIDS patients], burns.

C. adverse: bone marrow disorders, renal failure. If you have a diabetic, toxic epidermal necrolysis. hepatitis, stomatitis, crystalluria. megaloblastic anemia, hypoprothrombinemia, allergic myocarditis.

Drug: Coumadin interference: sulpha’s cause clotting

VIII. ANTITUBURCULAR & ANTIFUNGAL AGENTS

A. Anti-tuburcular agents:

1. TB: pathology & symptoms: Symptoms; coughing, hacking, night sweats.

Tuberculosis bacteria and illness is back on the rise due to cramped populations, Russian prisons, highly resistant strains, etc. Combination therapies for 6-24 months is the usual treatment. Not just a lung disease, although mostly a lung disease. Droplet/airborne spread

2. Prototype Isoniazid (INH)

action: inhibits cell-wall synthesis

use: TB treatment and prophylaxis

adverse: blood dyscrasias, hepatoxicity

Nursing Process

B. Antifungal Drugs

1. Causes of fungal infections: Usually fungal infections are super infections; can be focal or systemic.

2. Prototype: Fluconazole (Diflucan)

use: treat candida infections and meningitis

action: increases permeability of cell membrane

adverse: none known, No adverse [really?] but not for renal/hepatic impaired pts. N/V

IX. ANTIVIRAL NON-HIV DRUGS & UTI DRUGS

Viruses are tricky b/c: they’ve already invaded our cells, and don’t do their own metabolism, so they are difficult targets

A. Non-HIV Anti-Viral Prototype: Acyclovir sodium (Zovirax)

1. caution: electrolyte imbalance, children

2. use: treat HSV-2 and HSV-2

3. action: interferes with viral DNA synthesis

4. adverse: nephrotoxicity, bone marrow depression, renal failure

Acyclovere: HSV ½ [herpes] Serious adverse effects: renal, bone marrow, etc.

UTI drugs: UTI symptoms: fever, burning, frequency, discharge, etc. Elderly: confusion—oddly enough old people don’t have the burning sensation but they get altered LOC.

B. UTI Drugs: Nitrofurantoin (Furalan)

1. use: treat acute and chronic UTIs

2. action: inhibits bacterial enzymes and metabolism

3. adverse: superinfection, hepatotoxicity

C. Nursing Process

X. CASE SCENARIOS

A. Migrant laborer with chronic cough, night sweats

Community nursing: migrant worker w/ nightsweats and cough. Think: TB. Get an interpreter, figure out how to get the meds paid for. Test the family and give them prophylactic drugs.

B. 85 yo hospitalized female with MRSA in her sputum

85 yo F w/ MRSA in her sputum. Vancomycin or Gentomycin. Contact precautions, handwashing, etc. Don’t let your RN manager give you this pt and a post op pt in the same rotation.

C. 55 yo with pneumonia

55 yo with pneumonia: assess lung sounds, adequate hydration, sitting up, drugs are good. Supplemental O2.

Fluid in the pleural space: pleural effusion; why Margi couldn’t hear anything in the right base.

D. 74 yo with UTI admitted from SNF

74 yo w/ UTI admitted from a SNF. High risk, elderly, needs antibiotics.

Care Plans

As an experiment, I'm hosting care plans I've made online. Although we only have one clinical session left, we'll be writing these for 2 more years.

Impaired Walking:
http://docs.google.com/Doc?id=dgc7bfbt_1gxnmgx

Pain:
http://docs.google.com/Doc?id=dgc7bfbt_2cmpw65

Urinary Retention:
http://docs.google.com/Doc?id=dgc7bfbt_4fn3756

Impaired Movement:
http://docs.google.com/Doc?id=dgc7bfbt_7cs28xm

Impaired Tissue
http://docs.google.com/Doc?id=dgc7bfbt_8hn8jf7

Impaired Gas Exchange [pneumonia]
http://docs.google.com/Doc?id=dgc7bfbt_9qrmz9x

Pain again:
http://docs.google.com/Doc?id=dgc7bfbt_11g2zx3m

Impaired Vent Weaning:
http://docs.google.com/Doc?id=dgc7bfbt_13gvdmnz

Altered Thought Processes [TBI]:
http://docs.google.com/Doc?id=dgc7bfbt_15hbrx67

Impaired movement: quadriplegia r/t TBI
http://docs.google.com/Doc?id=dgc7bfbt_169stzjx

Spreadsheets for Clinical

My spreadsheet I use to grab information off the MAR:
http://spreadsheets.google.com/pub?key=pa-GnAC_jJcOSJd8TJvDHEw&output=xls

My sheet for lab tests at clinical, which I never use:http://spreadsheets.google.com/pub?key=pa-GnAC_jJcOB44Mx-_BJGw&output=xls

These are both formatted to allow a 1/2 inch margin for printing; most printers can handle that.

Cancer agents and BRM's

N203 CANCER AGENTS AND BIOLOGIC RESPONSE MODIFIERS

Upon completion of this class, the student will be able to:

1. Differentiate between cell-cycle specific and cell-cycle nonspecific drugs;

2. Identify general side effects and adverse reactions to chemotherapy agents;

3. State three ways the nurse can prevent absorption of chemotherapeutic agents;

4. Discuss the actions of the biologic response modifiers;

5. List adverse effects of interferons, colony-stimulating factors, and interleukin-2;

6. Describe the nursing process with safe administration of these agents.

I. Cancer

A. Influences on Cancer Development

1. environmental [chemicals, asbestos, radiation]

2. infective [viruses that cause tumors like Epstein Barr and Stomach ulcers, HPV, Herpes, Hep B and C]

3. diet [high fat]

4. genetic [BRCA 1 or BRCA 2 mutation]

“BRCA1 (breast cancer 1, early onset) is a human gene that belongs to a class of genes known as tumor suppressors, which maintains genomic integrity to prevent uncontrolled proliferation. The multifactorial BRCA1 protein product is involved in DNA damage repair, ubiquitination, transcriptional regulation as well as other functions. Variations in the gene have been implicated in a number of hereditary cancers, namely breast, ovarian and prostate. The BRCA1 gene is located on the long (q) arm of chromosome 17 at band 21….BRCA2 (Breast Cancer Type 2 susceptibility protein) is a human gene that is involved in the repair of chromosomal damage and belongs to a class of genes known as tumor suppressor genes. Tumor suppressor genes regulate the cycle of cell division by keeping cells from growing and dividing too rapidly or in an uncontrolled way. Although the structures of the BRCA1 and BRCA2 genes are very different, their functions appear to be similar. The proteins made by both genes are essential for repairing damaged DNA. The BRCA2 protein binds to and regulates the protein produced by the RAD51 gene to fix breaks in DNA. [wikipedia]”

B. Cancer causes: damage to DNA within cell; many mutations required

II. Cancer Drugs; ‘Chemotherapeutics’ aka ‘antineoplastics’

A. Cell-cycle Non Specific: don’t effect the cells during division: they are effective during the “G0” phase or resting phase between divisions…or they act at any time during the cell cycle.

B. Cell-cycle nonspecific: attack cancers when they are dividing, and during a specific phase of division.

C. Chemotherapy: most effective when able to kill cancer cells in all phases of cell cycle. Kills cancerous and normal cells.

1. systemic administration

2. used in conjunction with surgery and radiation

3. guided by protocols from research

4. length of treatment based on type and extent of malignancy, type of chemotherapy, expected side effects, and amount of time normal cells need to recover

5. combination therapy: combine drug types so that the cancer is attacked during all points of the cell cycle; so cycle specific and non-specific drugs are combined. This makes it likely that the effects are synergistic. This also avoids drug resistance by the tumors.

D. Adverse and side effects: hardest on quickly multiplying cells, esp. GI tract, vagina, and mucus membranes.

1. bone marrow suppression: resulting in low RBC, platelet, and WBC counts (anemia and neutropenia) Anemia: high BP, mental confusion/fatigue, high HR, high RR, and little peeing. Neutropenia: susceptible to infections. Thrombocytopenia: bruising, bleeding gums, etc.

2. GI disturbances: Anorexia, N/V, Diarrhea, Mucositis/Stomatitis. N/V caused by chemotherapies that trigger the CTZ, irritation to Gi, and radiation. Diarrhea caused by various effects and injury to the GI tract or infections. Mucositis is direct damage to the rapidly dividing tissues of the GI tract.

3. Alopecia: hair loss or thinning

4. Fatigue: due to stress, chemo, pain, infection, etc

5. Infertility: sometimes from severe radiation of the body—leaving sex cells useless.

E. Alkylating agent prototype: Cyclophosphamide (Cytoxan): Nitrogen Mustard

1. therapeutic uses: breast, lung, ovarian cancers; Hodgkin’s disease; leukemias; lymphomas

2. action: inhibits protein synthesis through interference with DNA replication

3. adverse effects: bone marrow depression [leukopenia, anemia, thrombocytopenia] cardiotoxicity, sterility, hepatotoxicity. Causes tissue necrosis if it infiltrates. Immunosuppresant.

F. Other types:

1. antimetabolites: disrupt metabolic processes and therefore enzyme synthesis. Treat head and neck, leukemia, breast, lung cancers, and non-hodgkin’s lymphoma. Need to give lots of “leukovorin calcium” to counteract effects on healthy cells.

2. antitumor antibiotics: certain antibiotics interfere with RNA and DNA production. Most of these are CCNS.

3. mitotic inhibitors: plant alkyloids that block division at the M cycle, so they are CCS. Made from periwinkle and yew. Periwinkle derivatives can be neurotoxic [they interfere w/ microtubules.] These can all cause common chemo adverse effects.

4. hormonal agents: corticosteroids [slow tumors and inflammation], androgens [testosterone to shink advanced breast cancers] and estrogen [slow the growth of hormone dependent tumors like prostatic and certain breast cancers,] antiestrogens [treats certain breast cancers,] antiandrogens [prostate cancer], etc.

5. liposomal chemotherapy: packages chemotherapeutic agents into synthetic fat globs called liposomes. The coating keeps the drug in the body longer and decreases side effects.

G. Nursing Process

Biologic Response Modifiers (BRMs)

A. Purpose: enhance body’s immune system. Immune proteins and chemicals produced w/ recombinant DNA tech and hybridoma tech [in which mice produce monoclonal antibodies.]

B. Interferons:

What I learned in micro: these are interesting because these are important in limiting virus replication, esp flu, hepatitis, herpes, colds, etc. We thought we could use them for all sorts of stuff, but they are deadly to the patient if over dosed/overused.

Interferons:

1. Use:

2: Action: has antiviral, antiproliferative, and immunomodulatory effects. Inhibits intracellular replication of viral DNA, tumor growth, and enhances natural killer cell activity.

2. Adverse effects: tachycardia, pallor, confusion, thrombocytopenia

C. Colony-stimulating Factors: These are ‘hematopoetic agents’ that manage/promote growth and differentiation of bone marrow stem cells—that create our RBCs, WBCs, etc. Therefore they do not attack tumors, but they do counteract those nasty chemo side effects, like prevent bone marrow suppression. That means greater doses of chemo can be given, aid in healing of suppressed marrow after chemo and transplant, promote immune cells to prevent infections.

1. Uses:

· decrease length of post-cancer treatment neutropenia

· permit delivery of higher doses of chemotherapy

· prevent severe thrombocytopenia with chemotherapy

2. Prototype: Filgrastim (Neupogen)

Action: increases neutrophils

Use: to prevent post-treatment infections

Life threatening Adverse effects: thrombocytopenia, MI

Adverse: Neutropenia, dyspnea, hematuria.

D. Epoeitin Alfa (Erythropoietin) (Procrit)

1. Action: stimulates RBC production in bone marrow

Life threatening adverse effects: CVA, MI

Adverse: Seizures, hyperkalemia, HTN

E. Nursing Process

Hot website: Rn Care Plans by NANDA Dx

Oh why didn't I find it sooner: a gold mine for my post clinical haze;

http://www1.us.elsevierhealth.com/MERLIN/Gulanick/Constructor/index.cfm

See: big fat list of NANDA Diagnoses, followed by the care plan, and rationales. All done!

Julie Danger

Pharma: Respiratory Agents

N203 RESPIRATORY AGENTS

Normal Pulmonary Function:

Co2 out, O2 in

Pressure changes, diffusion across membranes, pressure gradients. Compliance: alveoli and airways stretch. Naturally humidified to 100%. Surfactant; decreases surface tension between alveoli—who would rather collapse. Pons and respiratory centers [pons and medulla] in the brain, diaphragm innervated by the phrenic nerve, which respond to baro receptors and chemo receptors [that notice O2, CO2, H2 levels.] Peripheral chemoreceptors: carotid and aortic arch also check chemicals going by. These are responsive especially to O2. Volume: around 500mLs. People post op get atelectasis [collapsed alveoli], pneumonia, etc because it hurts to take a deep breath. Lungs love to get involved when pts come in for any pathology—being still in bed the lungs are likely to get pathological too. Pts lung sounds can change day to day. That’s the “outlier:” a pt who gets complications in the hospital and is there for 3 weeks instead of the 3 day stay for their surgery.

Concerns about using supplemental O2: low O2 is sensed by peripheral chemoreceptors [at aortic arch and carotids] and triggers increased ventilation. Putting a person on supplemental O2 can thereby have the opposite effect of depressing respiration.

Bronchial smooth muscles: are on bronchi and bronchioles, and respond to bronchoconstrictive PNS signals from the vagus nerve, and bronchodilate in response to SNS neurotransmitters [epinephrine.]

II. Drugs for Common Upper Respiratory Disorders

Runny nose: is rhinorrhea or rhinitis due to the common cold or to hayfever.

Pharm treatments for the common cold: antihistamine [H1] blockers, simpathomimetic decongestants, antitussives, and expectorants.

H1 versus H2: There’s H1 and H2—H2 are in the gastric, the H1 are in the upper respiratory. Histamine is an immune inflammatory agent released from the mast cells.

A. Antihistamines

2. Prototype: Diphenhydramine (Benadryl)

Action: compete with histamine for H₁ receptor sites, prevent histamine (allergic) response.

Indication: allergic rhinitis, itching, sleep aid, antitussive

Contraindication: acute asthmatic attack, severe liver disease

Adverse effects: agranulocytosis, hemolytic anemia, thrombocytopenia [so please don’t take this long term]

side effects: drowsiness, N & V, urinary retention, blurred vision, hypotension

patient teaching; avoid other CNS depressants, driving. Don’t take this long term.

Prototype: Loratadine: Claritin: has fewer side effects, it’s a second generation drug.

Action: compete with histamine for H₁ receptor sites, prevent histamine (allergic) response. Non-sedating b/c It has poor affinity to CNS H₁ receptors.

Use: Relief of symptoms of seasonal allergic rhinitis; idiopathic chronic urticaria [hives].

Adverse: Hypotension, hypertension, palpitations, syncope, tachycardia

Education: Avoid CNS depressants.

B. Decongestants

1. action: produce vascular constriction of nasal mucosal capillaries

2. administration: nasal spray or drops

3. caution; frequent use can lead to rebound nasal congestion from irritation of mucosa; use less than 5 days

4. adverse effect: HTN, hyperglycemia

Prototype: Sinex

Action: alpha-adrenergic agonist; mydriatic; decongestant. Potent, synthetic, direct-acting sympathomimetic with strong alpha-adrenergic and weak beta-adrenergic cardiac stimulant actions. Produces little or no CNS stimulation.

Use: Used topically for rhinitis of common cold, allergic rhinitis, and sinusitis. Also : Parenterally to maintain BP during anesthesia, to treat vascular failure in shock, mydriatic for ophthalmoscopic examination or surgery.

Adverse effect: HTN, tremor, sneezing, severe visceral or peripheral vasoconstriction

C. Antitussives [anti-cough]

Prototype: Dextromethorphan Hydrobromide (Robitussin DM)

Action: suppress cough reflex by inhibiting cough control center in medulla; reduces viscosity of tenacious/stringy secretions.

Use: Temporary relief of cough spasms in nonproductive coughs due to colds, pertussis, and influenza.

Contraindications: COPD, chronic productive cough

Adverse effects: hallucinations, CNS depression with very large doses

D. Expectorants

Best expectorant: adequate hydration. Expectorants loosen bronchial secretions so they can be expectorated

Prototype: Guaifenesin (Robitussin, Mucinex)

Action: Enhances reflex outflow of respiratory tract fluids by irritation of gastric mucosa.

Use: loosen mucus: Aids in expectoration by reducing adhesiveness and surface tension of secretions.

Contraindications: Cough due to CHF, ACE inhibitor therapy, or tobacco smoking.

Adverse effects: none. Nausea and dizziness, the end.

III. Drugs for Acute and Chronic Lower Respiratory Disorders

A. COPD

1. “Bronchial asthma is a COPD” [not included in Lemone/Burk book]

Asthma is bronchoconstriction set off by some stimulant—bronchial asthma is a chronic histamine reaction. “Clinically asthma is diagnosed when a patient has reversible airway obstruction." This is manifested by:

• Bronchospasm - wheezing, dyspnea, cough
• Mucous hypersecretion - mucus plugs, V/Q mismatch
• Airway edema - decreases airway diameter
• Airway inflammation - makes airway stiff (decreased compliance)
• Hyperactive airway - irritants can precipitate acute bronchospasm

Mild asthma is generally a seasonal condition or occurs sporadically. Wheezing and breathlessness may be experienced when triggered by events such as exercise. The attacks are mild, with symptoms presenting themselves only during the attacks. Treatment: a bronchodilator and used only to alleviate symptoms when they occur.

Moderate asthma usually occurs a couple times per week. Symptoms may present at night, may be triggered by exercise. An asthma attack may require emergency care. Treatment: may include a beta-agonist to be used when symptoms occur. Preventative treatment, such as an inhaled steroid, may be prescribed for administration between asthma attacks.

Severe asthma: continuous symptoms and/or frequent asthma attacks. These asthmatics must change their lifestyle to accommodate the condition. Overall activity levels are affected, and hospitalization and emergency care may be frequently required. Severe asthma has many triggers. Treatment: preventative medications, as well as medications to treat attacks.

Brittle asthma: is rare, unpredictable; attacks are very severe and can be life threatening. Treatment: Preventative and episodic medication is prescribed--Nebulizers and bronchodilators, and steroid tablets are used for long-term asthma maintenance and control.

2. Emphysema: oft from smoking but also sometimes from bad working conditions, coal, asbestos, steel workers. Also some genetic component from mutation of the Alpha-1-antitrypsin protein that prevents alveoli breakdown.

3. Chronic bronchitis: usually from smoking—these guys cough and rattle every morning and hack up sputum.

4. Factors Leading To Bronchoconstriction

· environment: what are they? Pollen, air pollution, temp changes, humidity, work, stifling perfume, etc.

· pollutants: what are they?

· allergic substances: what are they? Dust, animals, etc.

· drugs: such as? Asprin and NSAIDS [why? I don’t get it…]

COPD’ers get pneumonia b/c they don’t move as much air, low gas exchange, stagnant fluid in the lungs, all COPD’ers are always immunosuppressed because of chronic pathology. ‘Exacerbation’ is a flare up of symptoms: like pneumonia

B. Sympathomimetics

Prototype: Metaproterenol (Alupent)

Action: Hit Beta 2 receptors: bronchodilation, relaxation of smooth muscles of bronchi. “Potent synthetic beta-adrenergic agonist that acts selectively on beta₂-adrenergic receptors to relax smooth muscle of bronchi, etc.

Drug-drug interaction: increased with other sympathomimetics; Epinephrine, other sympathomimetic bronchodilators may compound effects of metaproterenol; MAO inhibitors, tricyclic antidepressants potentiate action of metaproterenol on vascular system; decreased effect of beta blockers

Given: PRN, Inhaler, PO, etc. Patient may use tablets and aerosol concomitantly.

Adverse effects: tremors, tachycardia, dysrhythmias, HTN, cardiac dysrhythmias, cardiac arrest, paradoxical bronchoconstriction.

RN Assessment: Listen to lungs before and after inhaler treatment.

Dyspnea: sense of breathlessness. DOE: dyspnea on exertion

PEOPLE ON ANTIINFLAMATORIES ARE ALWAYS AT RISK FOR INFECTION—BECAUSE WE ARE BLOCKING THEIR IMMUNE SYSTEM.

Inhaled drugs have local effects, therefore fewer systemic effects

C. Methylxanthine (Xanthine) Derivatives

Prototype: theophylline

Action: relaxes smooth muscle by direct action, particularly of bronchi and pulmonary vessels, but also GI.

Stimulates medullary respiratory center with resulting increase in vital capacity.

Stimulates myocardium, thereby increasing force of contractions and cardiac output,

Stimulates all levels of CNS, but to a lesser degree than caffeine.

Bad bad: narrow therapeutic range, not as effective as other inhalers— These are not inhaled, they are IV or PO.

Adverse effects: tachycardia, convulsions/seizure, dysrhythmias, cardiac arrest, CNS reactions, resp arrest, circulatory failure

D. Leukotriene Receptor Antagonists

1. effects of leukotrienes: inflammation in lungs:

2. Not to be used with acute asthmatic attack; used for prophylaxis and maintenance

Prototype: Montelukast ( Singulair)

Not for: acute asthma attack; used for prophylaxis and maintenance

Action: Leukotriene Receptor Antagonist; interrupts smooth muscle contraction/bronchoconstriction

adverse effects: none known!

Bronchodilators and Steroids are for acute asthma attack

E. Glucocorticoids (Steroids) for acute attack:

1. MDI [inhaler]

2. IV

3. PO

Beclomethasone (Vanceril) inhaler

Type: glucocorticoid, long acting

Use: for Rx of asthma, COPD, allergies

2. Action: suppresses inflammation and adrenal function

Side effects: Candidal infection of oropharynx, Dry mouth, itchy nose, etc.

Adverse: with excessive doses: symptoms of hypercorticism.

If ‘steroid dependent COPD’er,’ that’s a serious disease. If we see that, we have to make sure a steroid is ordered for them in order to keep their airways open. Don’t let them be abruptly stopped.

Hyperglycemia and hypertension always go with gluco [sugar] corticoids]

Mast Cell Stabilizer

F. Nedocromil: inhaler

Action: antiinflammatory; mast cell stabilizer: Inhibits activation of and mediators released from inflammatory cells (e.g., neutrophils, mast cells, monocytes).

Use: Don’t use for acute asthma attack. prophylaxis of bronchial asthma; inhibits histamine release; maintenance.

Adverse: none

Mucolytics: These are basically expectorants: they thin the mucus by acting like detergents. You need to see what the thickness of mucus is. If someone’s got thick mucus, you need to get them hydrated. Tenacious mucus is stringy.

IV. Case Scenarios

A. Your roommate has a cold, coughing all night so you can’t sleep. What drug and nondrug interventions are indicated?

Anti tussives, have them sit up, get OOB, vapo-rub,

B. Your patient has COPD with pneumonia. What drug and nondrug interventions are indicated?

Oxygen first. Get their pulse ox, in case they are CO2 retainers. Be upright for max lung expansion, or be comfortable. Use an incentive spirometer for breathing exercise. There’s a good chance the patient is dehydrated. Sympathomimetics, antibiotics, need to know the hx, might need steroids, need RT involved, and humidification. Think worst case: pt deteriorates and ends up on a vent.

C. Your 8 yo son plays CYO basketball. Every game he gets an asthma attack. What interventions are indicated?

Inhaler.

Objectives: Upon completion of this class, the student will be able to:

1. Compare antihistamine [blocks inflammatory immune response], decongestant [like sympathomimetics—sinex], antitussive [robitussin that depresses CNS cough center], and expectorant drug groups [mucinex or robitussin that thin mucus and irritate bronchial walls to get lung butter out];

2. Describe the nursing process with these agents;

3. Differentiate the drug groups used to treat COPD and asthma and the desired effects of each; glucocorticoids, xanthine derivatives [these are bad], mucolytics, Leukotriene Receptor Antagonists, sympathomimetics, Mast Cell Stabilizer

4. Contrast the therapeutic effects of these meds for for COPD and asthma; Leukotriene antagonists [leukotriene causes bronchconstriction, so we block it], glucocorticoids [block inflammatory response], Nedocromil [chills out the Mast cells by blocking their activating chemicals], antihistamines [blocks H1 receptors to prevent allergic reaction/inflammation], and mucolytics [get the lung butter thinner and expectorated]

5. Describe the nursing process with safe use of these agents.

205 IV and HIV day; class notes

N205 INTRAVENOUS THERAPY AND AIDS

Objectives: Upon completion of this class, the student will be able to:

1. Correlate the pathophysiologic alterations with the manifestations of HIV/AIDS infection;

2. Discuss normal regulation of fluids and electrolytes;

3. Describe the regulation of acid-base balance;

4. Discuss nursing responsibilities with IV therapy;

5. Describe nursing responsibilities with IV sites, IV tubing, and IV solutions;

6. Demonstrate correct technique for calculating drip rate of IV solutions.

I. AIDS: acquired immune deficiency syndrome

HIV: human immunodeficiency virus

From exposure to body fluid that’s infected/contaminated; vaginal secretion, breastmilk, blood, etc.

A. Pathology

1. Retrovirus infects cells with CD4 antigen [T–Helper cells and macrophages]

No longer a fatal disease but a chronic disease.

2. Enters cell and converts RNA to DNA with reverse transcriptase

3. HIV DNA integrated into host DNA

4. duplication of HIV during cell division

5. virus buds from cell surface, destroys host cell and spreads—you are left without enough surveillance in the body.

B. Manifestations

1. Primary HIV infection: flu like symptoms

2. Asymptomatic infection: no symptoms now but you become sero-positive—you’ve made antibodies that show up on a blood test.

3. Persistent generalized lymphadenopathy [lymph-gland-disease]

4. Acute symptoms: fever, weight loss, night sweats [like TB],

5. Opportunistic infections and cancer: as the CD4 cells die off, you’re up for all sorts of infections that are life threatening or not—cancers like Kaposi’s sarcomas.

Symptoms: stomatitis [sores in the mouth]

C. Diagnosis

1. CD4 T cell count

2. clinical symptoms

3. viral load

Nurse’s job: how do you know someone’s positive? It should be in their Hx, they should divulge it. It’s illegal to test for HIV w/o pt permission—whether a preop concern or a needlestick injury.

D. Interdisciplinary Care

1. Medications: reverse transcriptase inhibitors, protease inhibitors, HAART

2. Prevention

3. Assessment

4. Nursing Diagnoses: list four

Knowledge deficit r/t new diagnosis, community resources, AEB asking questions

Risk for infection r/t immunodeficiency

Anxiety r/t diagnosis, AEB frequent questions

Inbalanced nutrition r/t stomatitis, anorexia, nausea

Ineffective sexual patterns

Social isolation

5. Standard Precautions for healthcare provider safety

After today we hang piggyback’s and hang IV’s.

II. Body Fluids

Where is body fluid- interstitial and intracellular, somewhat extracellular, and we can’t really measure that.

How can you tell if someone is balanced or out of whack?

Assess:

Edema; fluid retention. Not as much output as input.

Capillary refill

I & O

A. Components

B. Movement

1. Osmosis

2. Diffusion

3. Filtration

C. Regulation: fill the tank or empty the tank

1. fluid intake

2. fluid output

3. maintaining homeostasis: who controls it? Kidneys, juxtaglomerular apparatus triggers the RAA, ADH, Aldosterone from hypothalamus/pituitary. Thirst center—people who don’t have thirst centers are low LOC people, and elders whose neurons are just old.

Normal potassium level should be around 3.5-5.0 , depending on the lab. Margi might test us on this.

What causes hyperkalemia? Supplements [micro K]

D. Regulation of Electrolytes

1. Why is this important?

2. What are they?

3. What do they do?

E. Acid Base Regulation: who does it? Look in the book at this, we will be tested on most normal blood gas abnormality [resp acidosis from hypoventilation] and on common lab values. The lungs and the kidneys.

1. Metabolic buffers

2. Respiratory Regulation

Lungs: blow off CO2 from cellular respiration:

CO2+H2O à H2CO2 à H+ à high H+

Hypoventilation means high CO2 holding which means high acid in the blood.

Cheyne-stokes respirations: a type of hyperventilation that blows off CO2

Blood gas values are covered in the book.

ABG’s: dissolved pressures of CO2 or O2 in arteries, not in veins. Normals:

pH: 7.35-7.45

pCO2: 35-45

pO2: 80-100

saO2: >95%

Bicarb: 22-26

3. Renal regulation

Kidneys: provide bicarbonate buffer system for the body. These take hours to days to make blood pH effects.

CBC tells us: WBC count. Check the electrolyte labs. CBC we really care about: BUN/Creatinine, H&H [hemoglobin and hematocrit]

F. Factors affecting body fluid, Electrolytes, Acid-base balance

1. Age: why?

2. Gender and body size-why?

3. Lifestyle-why?

4. Environmental temperature-why?

G. Fluid imbalances

1. Deficit

2. Third space syndrome

3. Excess

4. Edema

5. Dehydration

6. Overhydration

H. Electrolyte imbalances: Memorize the normal values for these, the symptoms of hypo and hyper’s

1. K

2. Na

3. Ca

4. Mg

5. Cl

6. PO4

Margi’s memorization of ABG’s: she memorizes the midpoint of all the ranges

7.4 [ph]

40 [CO2?]

100 [o2]

25 [bicarb]

100 [?]

I. Acid-base imbalances

1. Respiratory acidosis from hypoventilation (know this one)

2. Respiratory alkalosis from hyperventilation

3. Metabolic acidosis from excess body acids

4. Metabolic alkalosis from excess body bases

III. Nursing Management

A. Assessment:

1. History

2. PE

3. Daily weights

4. I & O

5. VS

6. Labs

B. Nursing Diagnoses: list four

C. Planning

D. Implementation

IV. IV Infusions

Who gets IV? Fluid managements, medications IV [esp antibiotics: by IVPB.]

Normal saline: 0.9%

Once I set up a piggyback bag: it needs to be labeled: pt, dose, time, date, my initials

A. Calculating Drip Factor

1. Nursing Responsibilities: calculate correct IV flow rate; regulate infusion; monitor client’s responses

Not all pts have IV machines hooked up—it drips w/o regulation. Ambulances don’t get these machines either. This is why you have to memorize how to calculate IV drip rate by hand. This will sometimes show up on entrance tests to hospitals.

You have to know the drip rate, and the drop factor on your bag. Drop factor is affected by the tubing diameter. So…the drop factor is the # of drops to deliver one mL of fluid in that particular tubing.

2. IV control device: know how to work it!!

3. Drip factor: drop factor: printed on package of IV tubing

· macrodrop: 10, 15 drops/ml

· microdrop: always 60 drops/ml

4. Calculate milliliters/hour

· divide total infusion volume by total infusion time in hours

· example: 1L over 8H. Divide 1000 ml by 8; equals 125 ml/hr

5. Calculate drops/minute:

a. Drops/min= total infusion x drop factor

total time of infusion in minutes

b. example: Infuse 1000 ml in 8 hours and the drip factor is 20 drops/ml

1000 ml x 20 = 41 drops/min

8 x 60 min (480 min)

6. . Factors affecting flow rate

· position of IV site

· position of tubing

· height of IV bag

· infiltration of IV solution or fluid leakage

B. Changing IV tubing or solution

1. Perform hand hygiene

2. set up necessary equipment

3. maintain sterile technique

4. flush new IV tubing with solution

5. attach to IV catheter

6. infuse at prescribed rate

IV’s are an RN function; LVN’s don’t typically do them.

If the machine is beeping; silence it while you problem solve.

The machine will freak out if there’s air in the line; it will tell you what’s going on and it will not run.

Hanging a piggy back bag: check the date of the tubing. make sure you have set the rollerclamp open on the IVPB, hang it higher than the IVF bag.

Primary vs secondary tubing.

Incompatibility issues: come up when 2 meds are in the same container. Not a problem running them sequentially in the same tubing. “Y site” incompatibility means don’t mix in the same tubes. Gentomycin is not compatible with anything.

Back flushing: to get air out of the tube. Do a little gravity thing—turn the tube upsidedown—this flushes from the Saline bag up to the piggy back. Back flush when hanging Gentomycin after Vancomycin and you want to re-use the tubing.

Why do docs order different fluids? Because they have their favorite flavors—its not about what the pt needs. Surgeons always order LR. Post op is often Dextrose which might be a good thing. We need to know why they are on which fluid.

Which fluid? Most people get isotonics. Sometimes people get a 3% NS, because their sodium is really low—or they want water out of the tissue for whatever reason. Colloids are hypertonic to pull water into the vessels in septic situations, etc. NS be cautious with CHF, perhaps.

Tubing can now be changed every 4 days, according to the CDC, some hospitals are different—some say 2 days. The CDC says 72 hours is the shortest amount of time b/c you’re interrupting the system and creating opportunity for infection. TPN: new bag, new tubing—b/c it’s like nutritional broth for bugs. Don’t put old tubing into a new site. If no label, assume its too old.

C. Nursing Responsibilities with IVs

1. Site patency

2. Correct IV solution and rate

3. client response to IV fluids

4. prevent complications

My job if pt has IV: I need to know the solution as MD ordered, if they still need that solution—is that solution the best for that pt with the current state. Make sure site is patent. Make sure rate etc are also appropriate. RN is still accountable for delivering an inappropriate order—even IVF. Make sure no infiltration—that it’s going iv, not intra tissue!

Site is sterile, inside of bags and tubes is sterile.

Do you need gloves on to hang IV? No.

D. Complications of IV Therapy

1. Phlebitis

2. Infiltration of solution

3. Extravasation of medication

4. Infection at site