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Pharmacology - Christi > Pharmacology Exam #2 Respiratory And Cardiac Ch. 29, 36-37, 41 > Flashcards

Pharmacology Exam #2 Respiratory And Cardiac Ch. 29, 36-37, 41 Flashcards

1
Q

What is the main function of the respiratory system?

A
  • deliver oxygen to and remove carbon dioxide from the cells of the body
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2
Q

Diseases of the LOWER respiratory tract

A
  • chronic obstructive disease (COPD)
    -Asthma (persistent and present most of the time despite treatment)
    -Emphysema
    -Chronic bronchitis

** All of these are airway obstruction of bronchioles………….treat with Albuterol

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3
Q

Bronchial Asthma

A
  • Recurrent and reversible shortness of breath
  • Occurs when the airway of the lungs become narrow as a result of:
  • Bronchospasm
  • Inflammation of the bronchial mucosa
  • Edema of the bronchial mucosa
  • Production of viscous
  • The aveolar ducts and alveoli remain open, but airflow to them is obstructed.
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4
Q

s/s: Wheezing and difficulty breathing

A

Bronchial Asthma

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5
Q

Four categories of Asthma

A
  • Intrinsic - occurring in patients with no
    history of allergies
  • Extrinsic - occurring in patients exposed to
    a known allergen
  • Exercise induced
  • Drug induced
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6
Q

Type of Asthma:

-Prolonged asthma attack that does not
respond to typical drug therapy
-May last several minutes to hours
-Medical emergency (911)

A

STATUS ASTHMATICUS

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7
Q
  • Continuous inflammation and low-grade infection of the bronchi
  • Excessive secretions of mucus and certain pathologic changes in the bronchial structure
  • Often occurs as a result of prolonged exposure to bronchial irritants
A

CHRONIC BRONCHITIS

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8
Q

-Included in COPD (which is no longer used as a term)
-air spaces enlarge as a result of the destruction of alveolar walls
- Caused by the effect of proteolytic enzymes released from leukocytes in response to alveolar inflammation
- the surface area where gas exchange takes place is reduced
- Effective respiration is impaired

A

EMPHYSEMA

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9
Q

These drugs relax bronchial smooth muscle, which causes dilation of the bronchi and bronchioles that are narrowed as a result of the disease process

A

BRONCHODILATORS

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10
Q

Three classes of Bronchodilators

A
  1. Beta-adrenergic agonists
  2. Anticholinergics
  3. Xanthine derivatives
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11
Q

Bronchodilators: Beta-Adrenergic Agonists

Short-acting beta agonist (SABA) inhalers

A

-Albuterol (Ventolin, ProAir)

ACUTE——-rescue inhaler
ex: pollen

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12
Q

Bronchodilators: Beta-Adrenergic Agonists

Long-acting beta-agonist (LABA) inhalers

A

-Salmetrol (Servent)

CHRONICH

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13
Q

Beta-Adrenergic Agonists: NEWEST LABA

LABA inhalers

A

-Indacaterol (Arcapta Neohaler)
- Vilanterol in conjuction with fluticasone (Breo Ellipta)
- Vilanterol in conjunction with the anticholinergic, umeclidinium (Anoro Ellipta)

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14
Q

-Used during ACUTE phase of asthmatic attacks
-Quickly reduce airway constriction and restore normal airflow
-Agonists, or stimulators, of the adrenergic receptors in the sympathetic nervous system
**Sympothomimetics

A

BRONCHODILATORS: BETA-ANDRENERGIC AGONISTS

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15
Q

BETA-ADRENERGIC AGONISTS: INTERACTIONS

A
  • diminish bronchodilation when nonselective beta blockers are used with the beta agonist bronchodilators
  • monoamine oxidase inhibitors (DO NOT WORK WELL WITH OTHERS)
  • sympathomimetics
    -monitor patients with diabetes; an increase in blood glucose levels can occur
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16
Q

Beta-Adrenergic Agonists:

ALBUTEROL (Proventil)

A
  • short-acting beta2-specific bronchodilating beta agonist
  • most commonly used drug in this class
  • must not be used too frequently
  • oral and inhalation use
  • inhalation dosage forms include metered dose inhalers (MDIs) as well as solutions for inhalation
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17
Q

Beta-Adrenergic Agonists:

SALMETEROL (Serevent)

A
  • long-lasting beta2 agonist bronchodilator
  • never to be used for acute treatment
  • used for the maintenance treatment of asthma and COPD and is used in conjunction with an inhaled corticosteroid
  • Salmeterol should never be given more than twice daily nor should the maximum daily dose (one puff twice daily) be exceeded
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18
Q

Adverse Effects of: Anticholinergics

A
  • dry mouth
  • nasal congestion
  • heart palpitations
  • gastrointestinal (GI) distress
  • headache
  • coughing
  • anxiety
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19
Q

Anticholinergics: Ipratropium (Atrovent)

A
  • oldest and most commonly used anticholinergic bronchodilator
  • available both as a liquid aerosol for inhalation and as a multidose inhaler
  • usually dosed twice daily
  • others
    -Tiotropium (Spiriva)
    -Aclidinium (Tudorza)
    -Umeclidinium (Incruse Ellipta)
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20
Q

Which medication will the nurse teach a client with asthma to use when experiencing an acute asthma attack?

A

ALBUTEROL (Ventolom)

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21
Q

Nonbronchodilating Respiratory Drugs

A
  • Leukotriene receptor antagonists (montelukast, zafirlukast, and zileuton LTRA
  • Corticosteroids (belcomethasone, budesonide, dexamethasone, flunisolide, fluticasone, ciclesonide, and triamcinolone)

*Bronchodilation
**Mucus production - block receptors

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22
Q

Leukotriene Receptor Antagonists (LTRAs)

A
  • nonbronchodilating (lung wheezing)
  • newer class of asthma medications
  • currently available drugs
    • Montelukast (Singulair)
    • Zafirlukast (Accolate)
    • Zileuton (Zyflo)
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23
Q

LTRAs: Mechanism of Action

A
  • Leukotrienes are substances released when a trigger, such as cat hair or dust, starts a series of chemical reactions in the body
  • Leukotrienes cause inflammation, bronchoconstriction, and mucus production
  • result: coughing, wheezing, shortness of breath
  • LRTAs prevent leikotrienes from attaching to receptors on cells in the lungs and in circulation
  • inflammation in the lungs is blocked, and asthma symptoms are relieved
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24
Q

LTRAs: Drug Effects

A

*By blocking leukotrienes:

  • prevent smooth muscle contraction of the bronchial airways
  • decrease mucus sectetion
  • prevent vascular permeability
  • decrease neutrophil and leukocyte infiltration to the lungs, preventing inflammation
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25
Q

LTRAs: Indications

A
  • prophylaxis and long-term treatment and prevention of asthma in adults and children 1 years of age and older
  • NOT meant for management of acute asthmatic attacks
  • Montelukast is also approved for treatment of allergic rhinitis
    -improve with their use is typically seen in about 1 week
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26
Q

LTRAs: Contradictions

A
  • known drug allergy
  • previous adverse drug reaction
  • allergy to povidone (shell fish), lactose, titanium dioxide, or cellulose derivatives is also important to note because there are inactive ingredients in these drugs
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27
Q

Corticosteroids (Glucicorticoids)

A

-antiinflammatory properties
- used for chronich asthma
- DO NOT relieve symptoms of acute asthma attacks
- may be admistered IV
- oral or inhaled forms
- inhaled forms reduce systemic effects
- may take several weeks before full effects are seen

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28
Q

Corticosteroids: Mechanism of Action

A
  • stabilize membranes of cells that release harmful bronchoconstricting substances
    - the cells are called leukocytes, or WBC
  • increase responsiveness of bronchial smooth muscle to beta-adrenergic stimulation
  • dual effect of both reducing inflammation and enhancing the activity of beta agonists
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29
Q

Corticosteroids: Mechanism of Action

A

-Corticosteroids have also been shown to restore or increase the responsiveness of bronchial smooth muscle to beta-adrenergic receptor stimulation, which results in more pronounced stimulation of the beta2 receptors by beta agonist drugs such as albuterol

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30
Q

Inhaled Corticosteroids

A

Fluticasone (Asmanex)

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31
Q

Inhaled Corticosteroids: Indications

A
  • Primary treatment of bronchospastic disorders to control the inflammatory responses that are believed to be the cause of these disorders
  • Persistent asthma
  • Often used concurrently with the beta-adrenergic agonists
  • Systemic corticosteroids are generally used only to treat acute exacerbations, or severe asthma
  • IV corticosteroids: acute exacerbation of asthma or other COPD
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32
Q

Inhaled Corticosteroids: Contraindications

A

** HIGH SUGAR CONTENT WILL CONTRIBUTE TO THRUSH

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33
Q

Inhaled Corticosteroids: Adverse Effects

A
  • Pharyngeal inflammation

** SUGAR EQUALS POOR WOUND HEALING

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34
Q

Corticosteroids: Nursing Implications

A

** ALWAYS TAKE BRONCHODILATOR BEFORE THE STEROID

  • Avoid exposure to conditions (allergens, smoke)
  • Adequate fluid intake
  • Complete medical treatment
  • Encourage clients to always check with the HCP before taking any other medication, including over-the-counter (OTC) medications, and herbal supplements
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35
Q

Nursing Implications: Corticosteroids

A
  • skin color
  • baseline vital signs
  • respirations (should be between 12 and 24)
  • respiratory assessment, including pulse oximetry
  • sputum production
  • allergies
  • history of respiratory problems
  • other medications
  • smoking history
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36
Q

Nursing Implications: Corticosteroids

A
  • teach clients to take bronchodilators exactly as prescribed
  • ensure that clients know how to use inhalers and MDIs and have client demonstrate use of the devices
  • monitor adverse effects
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37
Q

Nursing Implications: Corticosteroids

A

*Monitor for therapeutic effects:

-decreased dyspnea
- decreased wheezing, restlessness, and anxiety
- improved respiratory patterns with return to normal rate and quality
- improved tolerance
- decreased symptoms and increased ease of breathing

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38
Q

Nursing Implications: LTRAs

A
  • improvement should be seen in about 1
    week

-access liver function

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39
Q

Nursing Implications: Inhaled Corticosteroids

A
  • teach clients to monitor disease with a peal flow meter
    -encourage use of a spacer device to ensure successful inhalations
    -teach client how to keep inhalers and nebulizer equipment clean after use
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40
Q

Inhaler education

A
  • be sure that the client is able to self-administer
  • provide demonstration and return demonstration
  • ensure that the client knows the correct time intervals for inhalers
  • provide a spacer if the client has difficulty coordinating breathing with inhaler activation
  • ensure that the client knows how to keep track of the number of doses in the inhaler device
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41
Q

A client is prescribed 2 different types of inhaled medications for COPD. After administering the first treatment, how long should the nurse wait to administer the second medication?

A

Answer:

5 minutes

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42
Q

Antihistamines

A
  • H1 (histamine 1) - more airway
  • H2 (histamine 2) - more stomach

-Histamine 1 antagonists

-Allegra, Claritin, Zyrtec, diphenhydramine (Benadryl)
- Properties include: antihistamine, anticholinergic, sedative

-Histamine 2 agonists
- Pepcid

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43
Q

Decongestants

A
  • Adrenergic, Cholinergic, and Corticosteroids

-MOA - constricts blood vessels to nasal passageway preventing fluid that can cause mucus

** cause dehydration

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44
Q

Antitussives

A
  • drugs used to reduce cough
  • opioid and / or nonopioid (Codeine)
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45
Q

Expectorant

A
  • Drugs that promote expectoration of mucus
    - Mucinex
  • use in caution with asthmatics due to similar effect of Adrenergic

s/s: dehydration

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46
Q

Antitubercular Drugs

A
  • TB is caused by Myobacterium tuberculosis
  • Antitubercular drugs treat all forms of Mycobacterium (MTB)
    -TB is characterized by granulomas in the lungs: more specifically with inflammatory cells (macrophages and lymphocytes) that are walled off with defines boundaries
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47
Q
  • Lung (primary site)
  • brain
  • bone
  • liver
  • kidney
    genitourinary tract (GI)

-Aerobic bacillus
-Passed from infected patients to others (human to human, from cows/birds)

A

Mycobacterium (MTB) Infections

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48
Q

MTB Infections

A
  • droplets are expelled by coughing or sneezing, and they gain entry into the body by inhalation
    -Tubercle bacilli then spread to other body organs via blood and lymphatic systems
  • MTB: very slow-growing organism
  • more difficult to treat than most bacterial infections
    -dormancy: may test positive for exposure but are not necessarily infectious because of this dormancy process
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49
Q

How to diagnose TB

A

Step 1: Tuberculin skin test (Mantoux test)

Step 2: If skin test results are positive, then chest x-ray

Step 3: If chest x-ray shows signs of tuberculosis, then culture of sputum (100% accurate) or stomach secretions

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50
Q

TB Incidence Facts

A

1950’s TB in the US
-TB in patients coinfected with HIV

  • concern now: increasing number of multidrug-resistant tuberculosis (MDR-TB) cases
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51
Q

Multidrug-Resistant Tuberculosis (TB)

A
  • TB infects 1/3 of the words population
  • MDR-TB that is resistant to both isoniazid (INH) and rifampin
  • extensively drug resistant tuberculosis (XDR-TB): relatively rare type of MDR-TB
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52
Q

Antitubercular Drugs

A

First-Line Drugs:

  • Isoniazid (INH): primary drug used
    -Ethambutol
    -Rifampin
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53
Q

Antitubercular Drugs

A

Levofloxicin

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54
Q

Tuberculosis-Related Injections

A

-Purified protein derivative (PPD) (Mantoux)
-a diagnostic injection given intradermally in doses of 5 tuberculin units (0.1mL) to detect exposure on the TB organism
-positive results is indicated by induration (not erythema) at the site of injection

Bacille Calmette-Guerin (BCG)
-a vaccine injection derived from an inactivated strain of Myobacterium bovis

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55
Q

Antitubercular Drug Therapy: Considerations

A

-major effects of drug therapy: reduction of cough and therefore, reduction of the infectiousness of the patient
-successful treatment: several antibiotic drugs for at least 6 months and sometimes for as long as 12 months

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56
Q

When is the best time to collect a sputum culture of a TB patient who has been taking antitubercular drugs?

A

Answer:

In the morning

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57
Q

Antitubercular Drug Therapy: Consideration

A
  • adjust drug regimen after the results of susceptibility testing are known
  • monitor patient compliance closely during therapy
  • Problems with success therapy occur because of patient nonadherence….which causes increase incidence of drug resistant organisms
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58
Q

Mechanism of Action (TB) Drug Therapy)

A

Three Groups:

-Protein wall synthesis inhibitors

  • cell wall synthesis inhibitors
  • other mechanisms of action
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59
Q

Antitubercular Therapy

A

Effectiveness Depends on:
-type of infection (adjust based on specificity)
-adequate dosing
- sufficient duration of treatment
- adherence to drug regimen
Problems:
-drug resistant organisms
- drug toxicity
- patient nonadherence
MDR-TB: changes may need to be made half way through

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60
Q

TB Drugs

A

Ethambutol (Myambutol)

  • first bacteriostatic drug used in treatment of TB
  • diffuse into the mycobacteria and suppress RNA synthesis, inhibiting protein synthesis

Contradictions: optic neuritis, pediatric patients (younger than 13)

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61
Q

TB Drug

A

Isoniazid (INH)

TB drug of choice

Contradictions: with liver disease

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62
Q

TB DRUGS

A

Rifabutin, Rifampin, Rifapentine

  • Rifamycin antibiotics
  • also used to treat infections caused by non-TB mycobacterial species
  • adverse effect: turn urine, feces, saliva, skin, sputum, sweat, and tears a red-orange-brown color
  • oral use only
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63
Q

Adverse Effects of TB Drug

A

INH: peripheral neuropathy, hepatotoxicity

Ethambutol: retrobulbar neuritis, blindness

Rifampin: hepatitis; discoloration of urine, stools, and other body fluids

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64
Q

TB DRUGS: Nursing Implications

A

-perform liver function studies in patients who are to receive INH or rifampin (especially in older patients and those who use alcohol daily)
- patient education is crucial
-take medication exactly as ordered at the same time every day

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65
Q

TB DRUGS: Nursing Implications

A
  • Patient education is critical
  • remind patients that they are CONTAGIOUS during the initial period of their illness
    -Patients should not consume alcohol
    -Rifampin causes oral contraceptives to become ineffective
    -tell patients Rifampin will turn bodily fluids reddish-orange
    -Oral preps may be given with meals to reduce GI upset (even though recommendations are to take them 1-2 hours before meals)
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66
Q

TB DRUGS: Nursing Implications

A
  • monitor for adverse effects
    -fatigue, nausea, vomiting, numbness, and tingling of extremities, fever, loss of appetite, depression, and jaundice

-monitor for therapeutic effects
-x-ray = effective (check for granuloma decrease)

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67
Q

Fluid Balance

A

Total body water
-composed of:
-intracellular fluid (ICF)
-extracellular fluid (ECF)
-interstitial fluid (ISF)
-intravascular fluid (IVF)
-60% of adult human body is water
-plasma proteins exert constant osmotic pressure (anything not water or electrolytes)

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68
Q

Crystalloids

A

solution containing fluids and electrolytes that are normally found in the body
maintain the osmotic gradient between extravascular and intravascular compartments
NO PROTEINS

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69
Q

Colloids

A

Protein substance

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70
Q

Electrolytes

A

Principal ECF electrolytes
-cations (Na+)
Principal of ICF electrolyte
-Potassium (K+)

**Control the RAAS, SNS, Antidiuretic hormone system

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71
Q

Potassium

A

most abundant positively charged electrolyte inside cells

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72
Q

Sodium

A

most abundant positively charged electrolyte outside cells

Maintained through dietary intake of sodium chloride

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73
Q

Fluid Balance: Nursing Implications

A

assess baseline fluid volume and electrolyte status

assess baseline vital signs

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74
Q

Other Electrolytes

A

Magnesium
Chloride
Phosphorus
Calcium

Glucose - charged element which can impact Anion Gap

75
Q

What is hypertension?

A

“High blood pressure”

60 0r older: systolic pressure of greater than 150mmHg or Diastolic (bottom number) greater than 90 mmHg

Younger than 60 and those who have chronic kidney disease or diabetes: SBP greater than 140mmHg and DBP greater than 90mmHg

76
Q

What is a risk factor for coronary artery disease (CAD), cardiovascular disease (CVD)

A

Hypertension

**can cause Atherosclerosis

77
Q

Drug therapy for hypertension must be individualized.
What are the 7 main categories of drugs to treat hypertension?

A
  1. Diuretics (kidneys)
  2. Adrenergic drugs (week 2)
  3. Vasodilators (veins)
  4. Angiotensin-converting enzyme (ACE)
    inhibitors (RAAS)
  5. Angiotensin II receptor blockers (ARBs)
    (RAAS)
  6. Calcium channel blockers (CCB)
    *contractility
  7. Direct renin inhibitors (RAAS)
78
Q

5 subcategories of Adrenergic Drugs

A
  1. Adrenergic neuron blockers (central and
    peripheral
  2. Alpha2 receptor agonists (central)
  3. Alpha1 receptor blockers (peripheral)
  4. Beta receptor blockers (peripheral)
  5. Combo of Alpha1 and beta receptor
    blockers (peripheral)
79
Q

Centrally Acting Adrenergic Drugs

A

Clonide and Methyldopa(safe for
pregnancy/hypertension/anxiety)

  • stimulate alpha2-adrenergic receptors in
    the brain
  • decrease sympathetic outflow from the
    central nervous system (cause
    cholinergic response)
  • decrease norepinephrine production
  • stimulate alpha2-adrenergic receptors,
    thus reducing renin activity in the
    kidneys
    (RESULT IN DECREASE BLOOD PRESSURE)
80
Q

Peripherally Acting Alpha1 Blockers

A
  • Doxazosin
  • Prazosin
  • Terazosin

(block Alpha1 adrenergic receptors)
*decrease in Bp
* dilate arteries and veins
*Increase urinary flow rate

Use: Benign prostatic hyperplasia (BPH)

81
Q

Alpha2-Adrenergic Receptor Stimulators
(Agonists)

A
  • not typically described as first line drug
  • high incidence of unwanted adverse
    effects: fatigue, dizzy, orthostatic
    hypotension
  • Do not give to: p/t with head injury
  • last line of defense
  • DO NOT give if p/t has taken Benadryl
82
Q

Clonidine (Catapres)

A
  • used primarily for its ability to decrease
    blood pressure
  • used to manage Opioid withdraw
  • Oral and topical patch
  • Do not stop abruptly

*May lead to rebound hypertension

83
Q

Angiotensin-Converting Enzyme
(ACE) Inhibitors

A
  • Large group of safe and effective drugs
  • currently 10 ACE inhibitors
    -Often used as 1st line for heart failure and
    hypertension
  • may be combined with a thiazide diuretic
    or CCB
    -Block effect of Angiotensin
84
Q

Angiotensin-Converting Enzyme
(ACE) Inhibitors

End in PRIL

A
  • Captopril (Capoten) *PO (by mouth)
  • Enalapril (Lotensin) *PO & IV
    -Lisinopril (Prinivil) *PO & IV
85
Q

ACE Inhibitors: Mechanism of Action

A

-Inhibit ACE
-ACE converts angiotensin I (formed
through the action of renin to
angiotensin II)
- ALL: potent vasoconstrictor that induce
aldosterone secretion by the adrenal
gland
- Aldosterone: stimulates sodium and water
reabsorption, which can raise Bp

ACE inhibitors, thus low BP

86
Q

Primary Effects of the ACE Inhibitors

A

-Effects cardiovascular and renal systems
-Bp: reduce Bp by decreasing systemic
vascular resistance (SVR) *decreasing
force; lower Bp
-Prevent sodium and water resorption
- Diuresis: decrease blood volume and
return to the heart
-decrease preload (amount of blood that
goes back to the heart) or the left
ventricle end-diastolic volume
-Decrease work required by the heart

87
Q

Cardioprotective Effects of the ACE
Inhibitors

A

-ACE inhibitors decrease SVR(measure of afterload) and preload
-Used to prevent complications after MI
-Ventricular remodeling: left ventricular hypertrophy, which is sometimes seen after MI
-ACE inhibitors have been show to decrease mortality in p/t with HF
-Drugs of choice for hypertensive p/t with HF

88
Q

Renal Protective Effects of the
ACE Inhibitors

A

-ACE inhibitors: reduce glomerular filtration
pressure (GFR measure of blood flow
to kidneys, so useable blood)
-Cardiovascular drug of choice for p/t with
diabetes
-ACE inhibitors reduce proteinuria (this is
how it is renal protective)
-Standard therapy for diabetic patients to
prevent the progression of diabetic
nephropathy

89
Q

Renal Protective Ace Inhibitors

A

Only renal protective for diabetics

If diabetic has poor kidney function— than it is not protective

90
Q

ACE Inhibitors: Indications

A
  • Hypertension
  • HF (either alone or in combo with diuretics
    or other drugs)
  • Slow progression of left ventricle
    hypertrophy after myocardial
    infarction (MI) (cardioprotective
  • Renal protective in p/t with DIABETES
91
Q

ACE Inhibitors: Adverse Effects

A

-Fatigue
-Dizziness
-Hyperkalemia (know levels; high K can
cause harm)
-Cough
-Angiodema: rare but potentially fatal

*not indicated for African Americans (give
them ARB instead

92
Q

ACE Inhibitor: Adverse Effects

A

Note: First dose; hypotensive effect may
occur

A - angiodema
C - cough HELP REMEMBER!
E - everything else

93
Q

Angiotensin II Receptor Blockers (ARB)

A
  • Also referred to as angiotensin II
  • Well tolerated
  • Do not cause dry cough that is common
    with ACE Inhibitors
94
Q

Angoitensin II Receptor Blockers

A
  • Losartan (Cozaar)
  • Valsartan (Diovan

**Block Angiotensin II from being effective

95
Q

Angiotensin II Receptor Blockers:
Mechanism of Action

A
  • ARBs block vasoconstriction and the
    secretion of aldosterone (prevent Bp
    from rising)

Prevent vasoconstriction of ORGANS; not the same as arteries in ACE

96
Q

Angiotensin II Receptor Blockers:
Adverse Effects

A

-Fatigue
-Chest Pain
-Hypoglycemia
-Anemia
Hyperkalemia and cough are less likely to
occur with the ACE Inhibitors

97
Q

Losartan (Cozaar)

A

**Not safe for breastfeeding women and
should not be used in pregnancy
- beneficial in p/t with HF and hypertension
-used with caution in p/t with renal or
hepatic dysfunction and in p/t with
renal artery stenosis

98
Q

Calcium Channel Blockers:
Mechanism of Action

A

-primary use: HTN and angina
-cause smooth muscle relaxation by
blocking the binding of calcium to its
receptor, preventing muscle contraction
-result in:
-decreased peripheral smooth muscle
tone
-decreased SVP
-decreased Bp
- Nifedipine = safe for pregnancy

99
Q

Calcium Channel Blockers: Indications

A

-angina
-hypertension: amlodipine (Norvasc)
-dysrhythmias
-migraine headaches
-Raynaud’s disease
-prevent the cerebral artery spasms after
subarachnoid hemorrhage nimodipine

100
Q

Diuretics

A

-American Heart Assoc. says ACE is 1st line of heart treatment

-JNC 8 says 1st line antihypertensives (but that is old guideline)
-decreased plasma and extracellular fluid
volumes
- Results
-decreased preload
-decreased CO
-decreased total peripheral resistance
-Overall effect
-decreased workload of the heart and
decreased Bp
- Thiazide diuretics are the most commonly
used diuretics for hypertension

101
Q

Diuretics

*Act on Kidneys to raise production of
urnine

A

-Thiazide & Thiazide-like diuretics -
-Potassium sparing diuretics
-Loop diuretics

TEST: IV push of loop to fast can cause tinnitus (ringing in the ear)

102
Q

Diuretics

A

Lasix = Loop
HCTZ = Thiazide
Aldactone = Potassium sparing
Thiazide = Thiazide

103
Q

Vasodilators (dilate veins)

A

Hydralazine (Apresonline)

Minoxidil (Rogaine)
-for hair growth

104
Q

Vasodilators: Mechanism of Action

A
  • directly relax arteriolar or venous smooth
    muscle (or both)
    -Results in:
    -decreased SVR
    -decreased afterload
    -peripheral vasodilation
105
Q

Vasodilators: Adverse Effects

A

-Hydralazine: dizziness, headache, anxiety,
edema, diarrhea, hepatitis, systemic
lupus

106
Q

Vasodilators: Hydralazine (Apresoline)

A

-Orally: route of essential hypertension
-Injectable: hypertensive emergencies
-BiDil: specifically indicated as an adjunct for treatment of HF in African-American patients

107
Q

Vasodilators: Nursing Implications

A

-Before beginning therapy, obtain a
thorough health history
-Assess for contraindications to specific
antihypertensive drugs
-Assess for conditions that require caution
use of the drugs

108
Q

Vasodilators: Nursing Implications

A

-educate about missing a dose and taking EXACTLY line its ordered
-monitor Bp
-instruct patients to keep a journal
-do not stop abruptly
-oral forms should be given with meals
-administer IV forms with extreme caution
and use an IV pump

109
Q

Vasodilators: Nursing Implications

A
  • remind p/t that medication is only part of
    the therapy.
    -Encourage p/t to watch their diet, stress
    level, weight, and alcohol intake.
    -Avoid smoking and eating foods high in
    soduium
    -Encourage supervised exercise for elderly
    patients
110
Q

Vasodilators: Nursing Implications

A

-teach patients to change positions slowly to avoid syncope from postural hypotension
-instruct patients to report unusual shortness of breath; difficulty breathing; swelling of the feet; ankles; face; or around the eyes; weight gain or loss; chest pain; palpitations; an excessive fatigue

111
Q

Vasodilators: Nursing Implications

A

-male patients who take these drugs may
not be aware that impotence is
expected effect, and this may influence
compliance with drug therapy

112
Q

Vasodilators: Nursing Implications

A

-Hot tubs, showers, or baths; hot weather; prolonged sitting or standing; physical exercise; and alcohol ingestion may aggravate low Bp, leading to fainting and injury; p/t should sit or lie down until symptoms subside

  • p/t should never take OTC or any other meds without talking to HCP first
113
Q

ACE Inhibitors: Lab Values

A

–if creatinine is high = no ACE Inhibitors

**ACE inhibitors can cause hyperkalemia, so potassium levels need to be monitored
- Potassium level = 3.5-5.0

114
Q

General term for any process that stops bleeding

A

HEMOSTASIS

115
Q

Hemostasis that occurs because of the physiologic clotting factor

A

COAGULATION

116
Q

technical term for a blood clot

A

THROMBUS

117
Q

thrombus that moves through the blood vessels

A

EMBOLUS

118
Q

Rare genetic disorder where natural coagulation and hemostasis factors are limited or absent

A

HEMOPHILIA

119
Q

Two types of hemophilia that inhibit platelet aggregation

A
  • Factor VII deficiency

-Factor VIII/ or factor IX deficiency

120
Q

What are some of the most dangerous drugs used today.

Numerous factors can affect their action such as drug interactions and electrolyte interactions (potassium)

A

Drugs that effect coagulation

121
Q

Coagulation Modifier Drugs

A

Anticoagulants
-inhibit the action formation of clotting
factors
-Prevent clot formation (includes fibrin)
promotes clotting factor

122
Q

Coagulation Modifier Drugs

A

-Hemorheologic drugs
-alter platelet function without
preventing the platelets from working
-Thrombolytic drugs
-Lyse (break down) existing clots
-Antifibrinolytic or hemostatic
-promote blood coagulation

123
Q

Anticoagulants

A

-known as antithrombotic drugs
-have no direct effect on blood clot that is already formed

-Used prophylactically to prevent
-clot formation
-an embolus (dislodged clot)

124
Q

Embolus

A

Thromboembolitic events

-MI: embolus lodges in a coronary artery
-Stroke: embolus obstructs a brain vessel
-Pulmonary embolism: embolus in the
pulmonary circulation
-Deep vein thrombosis (DVT): embolus goes
to a vein in the leg

125
Q

Anticoagulants

A

Heparins - part 1
-action: inhibit clotting factor IIa (thrombin) and Xa

TEST: KNOW THIS

126
Q

Anticoagulants

A

Heparins - part 1
-unfractioned heparin: “heparin”
- low-molecular-weight heparins
(LMWHs)
-Enoxaparin
-Dalteparin (Fragmin)

127
Q

Heparin - part 2

A

-Unfractioned heparin (heparin)
-Relatively large molecule that is derived
from animal sources (PORK)
-Frequent lab monitoring for bleeding times
such as aPTT
-Heparin for catheter flush (10 to 100 units/mL): no monitoring is needed

128
Q

Heparin - part 3

A

-LMWHs
-Enoxaparin (Lovenox) and dalteparin
(Fragmin)
-Synthetic smaller molecular structure
-More predictable anticoagulant response
-Frequent lab monitoring of bleeding times
using tests such as aPTT not needed

TEST: what labs go with which drug & lab values….. look it up

129
Q

aPPT

A

activated partial thromboplastin time

130
Q

Anticoagulants

A

Coumarins
-action: inhibit vitamin K

Warfarin (Coumadin)
-inhibits vitamin K

Body needs vitamin K to produce prothrombin

TEST QUESTON!!!!!!!

131
Q

Anticoagulants: Factor Xa Drugs

A

End in…….. ABAN

132
Q

Anticoagulants

A

Direct thrombin inhibitors

-Action: inhibit thrombin (factor IIa)
-human antithrombin III (Thrombate)
-Lepirudin (Refludan)
-Argatroban (Agratroban)
-Bivalirudin (Angiomax)

133
Q

Anticoagulants: Indicators

A

Used to prevent clot formation in certain settings in which clot formation is likely
-MI
-unstable angina
-atrial fibrillation
-indwelling devices, such as mechanical
heart valves
-major orthopedic surgery

134
Q

Anitcoagulants: Contraindications

A

Do NOT GIVE Heparin for GI bleeding!
(TEST QUEST!!!!!!!!)

Drug allergy
Warfarin is strongly contraindicated in pregnancy

Heparin is safe for pregnancy

135
Q

Anticoagulants: Adverse Effects

A

-Bleeding

-May also cause:
-Heparin induced thromocytopenia
-Nausea, vomiting, abdominal cramps, thrombocytopenia, others

136
Q

Treatment: Toxic Effects of Heparin

A

-Symptoms: hematuria, melena (blood in stool), petechiae, ecchymosis, and gum mucous membrane bleeding
-stop drug immediately
-IV protamine sulfate: 1mg of protamine can reverse the effects of 100 units of heparin

TEST»»> KNOW THUS!

137
Q

Treatment: Toxic Effects of Warfarin

A

-discontinue
-may take 36-42 hours before the liver can resynthesize enough clotting factors to reverse the warfarin effects
-vitamin K1 (phytonadione) can hasten the return to normal coagulation
-high dose vitamin K (10mg) given IV will reverse the anticoagulation within 6 hours

Reversal vitamin K (caution: warfarin resistance will occur for up to 7 days)

TEST KNOW THIS!!!!!!

138
Q

Drug Interactions: Anticoagulants

A

-enzyme inhibition of metabolism
-displacement of the drug from inactive
protein binding sites
-decrease in vitamin K absorption or
synthesis by the bacterial flora of the
large intestines
-alteration in the platelet count or activity

139
Q

Argatroban

A

-synthetic direct thrombin inhibitor
-used for active HIT and percutaneous coronary intervention procedures in p/t at risk for HIT
-ONLY give IV

140
Q

Dabigatran (Pradaxa)

A

-first oral direct thrombin that is approved for prevention of strokes and thrombosis in p/t with nonvalvular atrial fibrillation
-specifically and reversibly binds to both free and clot-bound thrombin
-dose dependent on renal function
-adverse effects: bleeding, GI bleeding
-no coagulation monitoring is required

141
Q

Enoxaparin (Lovenox)

A

Prototypical LMWH
-greater affinity for factor Xa than for factor
lia
-Higher degree of bioavailability and longer
elimination half-life
-lab monitoring is not necessary die PT/INR,
but is required for kidney function
-injectable form
-used for prophylaxis and treatment
-pre-filled syringes
-do not expel air bubble

142
Q

Heparin

A

Natural anticoagulant obtained from the lungs or intestinal mucosa of pigs
-10-40,000 units/mL
-DVT prophylaxis: 5000 units subcu 2-3 times a day; does not need to be monitored when used for prophylaxis
-when heparin is used therapeutically (for treatment) continuous IV infusion.

**measurement of aPTT (usually every 6 hours until therapeutic effects are seen) is necessary

143
Q

Rivaroxaban (Xarelto)

A

-first oral factor Xa inhibitor
-used for prevention of strokes in patients with a-fib; post op thromboprophylaxis with ortho surgeries; treatment of DVT and PE

Adverse reactions: peripheral edema, dizziness, headache, bruising, diarrhea, hematuria, and bleeding

144
Q

Warfarin (Coumadin)

A

-most commonly prescribed oral
anticoagulant
-careful monitoring of the prothrombin
time/international normalized ratio (PT?
INR)
-a normal INR (with warfarin) ranges from 2
to 3.5 depending on indication of the
drug
-many drug interactions
-dietary considerations

145
Q

Reversal for Warfarin

A

Vitamin K

146
Q

Antiplatelet Drugs

A

work to prevent platelet adhesion at the site of blood vessel injury

-Prevent platelet adhesion
-Aspirin
-Clopidogrel (Plavix)

147
Q

Antiplatelet Drugs: Indications and Adverse Effect

A

-antithrombotic effects (clotting)

-Adverse effects
-vary according to drug, bur BLEEDING is common (if someone is bleeding)

148
Q

Clopidogrel (Plavix)

A

-most widely used ADP inhibitor (adenosine diphosphate)

-oral use
-Prasugrel (Effient),

Many drug interactions

149
Q

Thrombolytic Drugs

A

-drugs that break down, or lyse, preformed
clots
-older drugs
-Streptokinase and urokinase
-current drugs
- Alteplase (activase, cathflo activase)

TPA»»active stroke

150
Q

Thrombolytic Drugs

A

Break Down Clot in blood vessel quickly

TEST!!!! KNOW

151
Q

Thrombolytic Drug: Indications

A

-acute MI
-arterial thombolysis
-DVT
-occlusion of shunts or catheters
-pulmonary embolus
-acute ischemic stroke

152
Q

Thrombolytic Drugs: Adverse Effects

A

Bleeding

TEST!!!!!

153
Q

Alteplase (Activase)

A

t-PA made through recombinant DNA techniques (t-PA 2yr gap if given prior)
-fibrin specific so does not produce a systemic lytic state
-present in the body in natural state
-very short half life (5 minutes)

Indications:
-stroke, MI
-smaller doses to flush clogged IV or arterial lines

154
Q

Antifibrinolytic Drugs

A

*if someone is bleeding out

-prevent lysis of fibrin
-result in promoting clot formation
-Aminocaproic acid (Amicar)
-Tranexamic acid (Cyklokapron)
Desmopressin

155
Q

Antifibrinolytic Drugs: Adverse Effects

A

Rare reports of thromotic (blood clot) events

156
Q

Antifibrinolytic Drug: Nursing Implications

A

Assess:
-patient history, medication history, allergies
-contraindications
-baseline vital signs, lab values
-potential drug interactions
-history of abnormal bleeding conditions

157
Q

Heparin: Nursing Implications

A

-IV doses are usually double checked with
another nurse
-do not give subcutaneous dose within 2
inches of:
-the umbilicus, abdominal incisions,
open wounds, scars, drainage
tubes, or stomas
-DO NOT aspirate subcutaneous injections
or massage the injection site (may cause
hematoma formation)

158
Q

Heparin: Nursing Implications

A

-IV doses may be given by bolus or IV infusions.
-anticoagulants effects are seen immediately
-lab valued are done daily to monitor coagulation effects aPTT
-protamine sulfate can be given as an antidote in case of excessive anticoagulation

159
Q

LMWHs: Nursing Implications

A

Low Molecular Weight Heparin
-given subcutaneously in the abdomen
-rotate injection sires
**Protamine sulfate can be given as as antidote

160
Q

Warfarin (Coumadin): Nursing Implications

A

-effects take several days
-monitor PT/INR
-Antidote is vitamin K***

161
Q

Warfarin: Nursing Implications

A

Avoid all herbal products!

TEST QUES

162
Q

Anticoagulant: Patient Education

A

-measures to prevent bruising, bleeding, and tissue injury
-wearing a medical alert bracelet
-avoiding foods high in vitamin K (tomatoes, dark leafy green vegetables)

163
Q

Drug Therapy for HF

A

-Positive Inotropic Drugs: INCREASE force of myocardial contraction
-Positive Chronotropic Drugs: INCREASE heart rate
Positive Dromotropic Drugs: ACCELERATE cardiac conduction
-ACE’s, ARB’s, BB, Diuretics

164
Q

Positive Inotropic Drugs

A

Dobutamine - greater force, more blood that comes out of the heart

165
Q

Cardiac Glycosides

A

Positive inotropic effect - increased force and velocity of myocardial contraction (without an increase in oxygen(heart pain) consumption

166
Q

Cardiac Glycosides

A

Negative chronotropic effect - reduced heart rate

167
Q

Cardiac Glycosides

A

Negative dromotropic effect - decreased automaticity at SA node, decreased AV nodal conduction, and other effects

168
Q

Cardiac Glycosides

A

-increased stroke volume
-reduction in heart size during diastole
-decrease in venous BP and vein engorgement
-increase in coronary circulation
-decrease in exertional and paroxysmal noturnal (diff breathing at night)
-improved system control, quality of life, and exercise tolerance
-no apparent reduction in mortality

169
Q

Cardiac Glycosides

A

Dogoxin (Lanoxin)
-drug levels must be monitored
-0.5 to 2 ng/mL
-low potassium levels increase its toxicity

KNOW THIS!!!

170
Q

Digoxin Toxicity

A

Digoxin immune Fab (Digibind) therapy
-life-threatening cardiac dysrhthias
-life-threatening digoxin overdose

Digiband - REVERSAL

171
Q

Drugs for Angina

A

Nitrates or nitrites (expand cardiac arteries)
Beta Blockers
Calcium channel blockers (CCBs)

172
Q

Nitrates and Nitrates

A

Available forms
-sublingual (only 3 doses allowed before needing new order; 5 min between doses)
-chewable tabs
-oral capsules/tabs
-IV solutions
-Transdermal patches
-oitnments
-Translingual sprays

Morphine reduces demand on the heart

173
Q

Nitrates and Nitrites: Mechanism of Action

A

Cause vasodilation because of relaxation of smooth muscles

Result: oxygen to ischemic myocardial tissue

174
Q

Nitrates and Nitrites: Indications

A

-treat stable, unstable, and vasospastic angina
-rapid-acting forms
-treat acute anginal attacks
-sublingual tabs; IV infusion
-long-acting form
-prevent anginal episodes

175
Q

Nitrates: Contraindications

A

-known drug allergy
-severe anemia
-closed-angle glaucoma
-hypotension
-severe head injury
-use of the erectile dysfunction drugs silenafil (viagra), tadaladil (Cialis), and vardenadil (Levitra

176
Q

Nitrates: Adverse Effects

A

-Headaches
-Reflex tachycardia
-postural hypotension
-skin irritation with topical application
-tolerance may develop

177
Q

Antidysrhythmic Drugs

A

Dysrhythmia
any deviation from the normal rhythm of the heart

Arrhythmia
“no rhythm” which implies asystole

178
Q

Vaughan Williams Classification:
Mechanism of Action & Indications

A

Class III - amiodarone, sotalol

179
Q

Amiodarone (Cordarone, Pacerone)

A

Class III
-blocks both alpha and beta adrenergic receptors of the sympathetic nervous system

uses: effective antidysrhythmic
indications: management of dysrhythmias
adverse effects: visual halos, photosensitivity

180
Q

Verapamil (Calan)

A

Class IV

results in dramatic effects on the AV node

181
Q

Antilipemics: HMG-CoA Reductase Inhibitors (Statins)

A

Statins

Patients with LDL cholesterol levels greater than or equal to 190 mg/dl
HDL higher than 150

LDL levels between 70 and 189mg/dl

182
Q

Antilipemics: HMG-CoA Reductase Inhibitors (Statins)

A

Statins

Patients with LDLcholesterol levels

183
Q

Statins

A

Simvastatin (Zocor)

Avorvastatin (Lipitor)

184
Q

Rhabdomyloysis

A

-breakdown of muscle protein
-myoglobinuria: urinary elimination of the muscle protein myoglobin
-can lead to acute renal failure and even death

if muscle pain exists—–no Statins—–could cause myoglobinuria

Pharmacology - Christi (2 decks)

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