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Pharmacology for Nurses > Exam 2 Material > Flashcards

Exam 2 Material Flashcards

1
Q

Allergic Rhinitis

A

Exposure to allergen (antigen) triggers mast cells to release histamine and several other chemical mediators, causing common allergy symptoms

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2
Q

Drugs for prevention of allergic rhinitis

A

Leukotriene modifiers Mast cell stabilizers Antihistamines: H1 receptor blockers (antagonists) Intranasal corticosteroids

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3
Q

Drugs for relief of allergic rhinitis

A

Decongestants (most are sympathomimetics)

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4
Q

What are anticholinergic effects?

A

Acetylcholine is a neurotransmitter that affects muscular contraction (including cardiac muscle) and endocrine function Anticholinergic effects (think blocking the effects of acetylcholine) include dry mouth, constipation, urinary retention, increased heart rate, dilated pupils, blurred vision, decreased sweating

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5
Q

Therapeutic class of diphenhydramine (Benadryl)

A

Antihistamine; allergy

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6
Q

Pharmacological class of diphenhydramine (Benadryl)

A

H1 receptor blocker/antagonist

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7
Q

Indications for diphenhydramine (Benadryl)

A

Allergies, motion sickness, insomnia, pruritus (itching), Parkinson’s disease

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8
Q

MOA of diphenhydramine (Benadryl)

A

H1 receptor antagonist - blocks action of histamine

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9
Q

Cautions for diphenhydramine (Benadryl)

A

Elderly more likely to experience delirium, increased heart rate Children more likely to have paradoxical excitation

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10
Q

Adverse effects of diphenhydramine (Benadryl)

A

Drowsiness (can develop tolerance to this), dry mouth, increased heart rate (anticholinergic effects)

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11
Q

Interactions of diphenhydramine (Benadryl)

A

Avoid concurrent use with other CNS depressants

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12
Q

Therapeutic class of fluticasone (Flonase)

A

Anti-inflammatory (includes skin conditions), allergic rhinitis, asthma

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13
Q

Pharmacological class of fluticasone (Flonase)

A

Corticosteroid

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14
Q

Indications of fluticasone (Flonase)

A

Allergic rhinitis

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15
Q

MOA of fluticasone (Flonase)

A

Decrease inflammation in nasal mucosa

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16
Q

Adverse effects/interactions of fluticasone (Flonase)

A

Burning sensation when spraying, epistaxis (nose bleed)

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17
Q

Therapeutic class of oxymetazoline (Afrin)

A

Decongestant

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18
Q

Pharmacological class of oxymetazoline (Afrin)

A

Sympathomimetic

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19
Q

Indications of oxymetazoline (Afrin)

A

Allergic rhinitis, nose bleeds, nasal congestion

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20
Q

MOA of oxymetazoline (Afrin)

A

Alpha1 adrenergic agonist (causes vasoconstriction of blood vessels in the nasal mucosa and drying of mucous membranes)

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21
Q

Caution for oxymetazoline (Afrin)

A

Use with caution in people with HTN, thyroid disorders, diabetes, and heart disease

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22
Q

Adverse effects of oxymetazoline (Afrin)

A

Rebound congestion, dry/stinging of nasal mucosa

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23
Q

Nursing implications of oxymetazoline (Afrin)

A

Instruct clients not use use for more than 3 days

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24
Q

What is the action of alpha 1 - adrenergic receptors agonists

A

Vasoconstriction

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25
Q

What is the action of alpha2 adrenergic agonists

A

Inhibits the release of norepinephrine (negative feedback)

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26
Q

What is the action of beta1 adrenergic agonists

A

Increased HR and contractility

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27
Q

What is the action of beta2 adrenergic agonists

A

Relaxation of smooth muscle in bronchioles, uterus, GI tract, and bladder

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28
Q

What causes a cough refelx

A

Cough center is located in the medulla; it is a symptom of an underlying condition

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29
Q

What are antitussives

A

Suppress cough by raising cough threshold or anesthetizing stretch receptors in the lungs

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30
Q

What are expectorants

A

Simulate mucous flow and decrease viscosity of secretions; make cough more productive

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31
Q

What are mucolytics

A

Break down mucus; used for COPD and cystic fibrosis

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32
Q

What is asthma

A

A chronic pulmonary disease characterized by acute bronchoconstriction and inflammation of the airways, leading to increased mucus production and airway obstruction

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33
Q

What are the goals to asthma therapy?

A

Terminate acute bronchospasm Reduce frequency of asthma attacks

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34
Q

Why may IV medications be necessary during a severe asthma attack?

A

Mucus is coating the lungs and the medication is unable to reach the site of action

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35
Q

What type of drugs are given during an acute bronchospasm?

A

Beta2 adrenergic agonists Leads to bronchodilation Has few adverse effects (increased heart rate, tremors) Short acting beta agonists (SABA) rescue inhaler: has rapid onset and effective for 2-6 hours Albuterol is an example

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36
Q

When are anticholinergics given in asthma?

A

Can be used in conjunction with beta 2 adrenergic agonists Not as quick or as effective as B2 adrenergic agonists Few adverse effects Atrovent is an example

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37
Q

When are systemic corticosteroids used in asthma?

A

IV - hospital

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38
Q

Maintenance therapy of asthma includes what drug types?

A

Long acting beta agonists (LABAs) Corticosteroids Mast cell stabilizers Leukotriene modifiers Methylxanthines Biologics/monoclonal antibodies

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39
Q

What do long acting beta agonists (LABAs) do

A

Slower onset (20-60 min) Will not help during an acute asthma attack Causes bronchodilation Examples: salmeterol (Serevent), formoterol (Foradil)

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40
Q

What do corticosteroids do in asthma?

A

Treat inflammatory component Most effective drug for prevention of acute attacks Few adverse effects when inhaled Can cause oral thrush (rinse mouth after use) Must use daily; can take 4-8 weeks for maximum effect Oral/Iv routes used in severe cases Examples: fluticasone (Flovent), budesonide (Pulmicort), beclomethasone

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41
Q

What do mast cell stabilizers do for asthma?

A

Inhibit the release of histamine from mast cells Examples: cromolyn (Intal)

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42
Q

What do leukotriene modifiers do for asthma?

A

Modify the action of leukotrienes, which are chemical mediators of inflammation Only available orally Adverse effects: headache, GI symptoms, anxiety, depression, suicidal behavior/thoughts Example: montelukast sodium (Singulair)

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43
Q

What do methylxanthines do for asthma?

A

Bronchodilator Narrow margin of safety Many drug interactions Adverse effects: N/V, CNS stimulation, dysrhythmias Examples: theophylline (Theo-dur), amnophylline

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44
Q

What do biologics/monoclonal antibodies do for asthma?

A

Target inflammation pathways involving IgE (antibodies) Examples: omalizumab (Xolair) Tend to be expensive

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45
Q

What is COPD?

A

Chronic, progressive lung disease characterized by inflammation and excess mucus (chronic bronchitis) and alveolar dilation/loss of elasticity (emphysema)

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46
Q

What medications are used for COPD?

A

LABAs Anticholinergic bronchodilators Inhaled corticosteroids Mucolytics and expectorants Several combination drugs Oxygen

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47
Q

What medications are avoided/used with caution in COPD??

A

Beta-adrenergic antagonists (causes bronchoconstriction) Respiratory depressants (opioids)

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48
Q

When taking more than one inhaler, which inhaler should be taken first?

A

Bronchodilator should be taken first to open up bronchioles and give more surface area for other medications to work

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49
Q

What does the autonomic nervous system control?

A

Involuntary responses 2 Divisions: sympathetic and parasympathetic

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50
Q

What are parasympathetic responses?

A

Constrict pupils Stimulate saliva Slow heart beat Constrict airways Stimulate activity of stomach Inhibit release of glucose; stimulate gallbladder Stimulate activity of intestines Contract bladder Promote erection of genitals

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51
Q

What are sympathetic responses?

A

Dilate pupils Inhibit salivation Increase heartbeat Relax airways Inhibit activity of stomach Stimulate release of glucose; inhibit gallbladder Inhibit activity of intestines Secrete epinephrine and norepinephrine Relax bladder (prevents urination) Promote ejaculation and vaginal contraction

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52
Q

What is a neurotransmitter?

A

A chemical substance that transmit a nerve impulse across a synapse, creating activation at a receptor site Includes: GABA AcH Dopamine Serotonine Histamine Many drugs have identical or similar chemical structures to neurotransmitters and work by enhancing or blocking the activity of the neurotransmitter

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53
Q

What are autonomic drugs?

A

Cholinergic/parasympathomimetic/cholinesterase inhibitors Cholinergic blockers/anticholinergics Adrenergics/sympathomimetics Adrenergic blockers

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54
Q

What do cholinergic/parasympathomimetics/cholinesterase inhibitors do?

A

Activation of the parasympathetic nervous system Rest and digest AcH is a neurotransmitter involved that will create a parasympathetic response Direct acting and indirect acting drugs

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55
Q

What do cholinergic blockers/anticholinergics do?

A

Inhibit parasympathetic nervous system

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56
Q

What do adrenergic/sympathomimetics do?

A

Activation of the sympathetic nervous system (fight or flight)

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57
Q

What do adrenergic blocker do?

A

Inhibit sympathetic nervous system

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58
Q

What are some adverse effects of cholinergic/parasympathomimetic/cholinesterase inhibitors?

A

Increased salivation Sweating Abdominal cramps Bradycardia Hypotension (due to slowing of the heart) Wheezing (constriction of bronchioles)

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59
Q

What are some direct acting cholinergics?

A

Bethanechol: stimulates bladder and GI tract after general anesthesia Pilocarpine: decreases intraocular pressure in acute glaucoma; treatment of dry mouth

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60
Q

What are some indirect acting cholinergics?

A

Donepezil (Aricept): increases avilability of AcH in Alzeimer’s Edrophonium (Tensilon): facilitates the diagnosis of Myasthenia Gravis (temporarily improves muscle strength)

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61
Q

Tensilon Test

A

Give Tensilon to a patient to temporarily increase AcH. Patient will get muscle strength back if they have Myasthenia Gravis. MG blocks AcH causing extreme fatigue and weakness in the arm and leg muscles, difficulty with chewing and speech.

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62
Q

What do cholinergic blockers (anticholinergics) do?

A

Block action of acetylcholine (specifically muscarinic receptors), mimicking the fight or flight response.

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63
Q

Therapeutic class of atropine?

A

Antidysrhythmic, mydriatic, antidote of anticholinesterase posisoning

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64
Q

Pharmacologic class of atropine

A

Anticholinergic

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65
Q

What do beta adrenergic blockers do?

A

Lower heart rate and blood pressure Atenolol, metoprolol

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66
Q

MOA of atropine

A

Blocks cholinergic (muscarinic) receptors, causing increased heart rate, decreased GI motility, mydriasis, bronchodilation, and decreased secretion from glands (salivation)

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67
Q

Adverse effects of atropine

A

Dry mouth, constipation, urinary retention, tachycardia, blurred vision

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68
Q

Contraindications of atropine

A

Clients with glaucoma

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69
Q

What do adrenergic (sympathomimetics) do?

A

Activation of sympathetic nervous system; fight or flight response. Norepinephrine is the neurotransmitter. Effects depends on what adrenergic receptor is stimulated (alpha1, alpha2, beta1, beta 2)

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70
Q

What does epinephrine stimulate?

A

Adrenalin stimulates alpha1 and beta receptors; used with asthma, cardiac arrest, allergic reactions

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71
Q

What does albuterol stimulate

A

Beta 2 receptors; used with asthma

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72
Q

What does clonidine stimulate?

A

Alpha 2 receptors; used with HTN Inhibits the release of the neurotransmitter

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73
Q

What are nursing considerations for clients taking adrenergics?

A

Have patients check with provider before taking OTC with the adrenergic Most significant effects relate to cardiovascular system (report chest pain, dizziness, palpitations) Monitor for urinary retention Monitor IV site for extravasation (tissue damage if it leaks into the tissue) Chewing gum/sucking hard candies can help dry mouth

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74
Q

What do adrenergic blockers do?

A

Inhibit sympathetic nervous system (similar to “rest and digest”)

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75
Q

What do alpha 1 adrenergic blockers do?

A

Relax vascular smooth muscle Doxazosin, prazosin

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76
Q

What do beta adrenergic blockers do?

A

Lower heart rate and blood pressure Atenolol, metoprolol

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77
Q

What is cholesterol?

A

A lipid that plays a key role in the development of atherosclerosis (plaque build up on the lining of the arteries). Contributes to angina, MI, and stroke (CVA)

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78
Q

What is atherosclerosis?

A

Narrowing of the arteries

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79
Q

What is arteriolosclerosis?

A

Hardening of the arteries

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80
Q

What is hyperlipidemia?

A

HPL is high lipid levels in the blood. It is a broad term Often there are other comorbidities (heart failure, diabetes, coronary artery disease)

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81
Q

What is hypertriglycermia?

A

High triglyceride levels More specific

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82
Q

Are triglycerides cholesterol?

A

NO, they are a lipid. Cholesterol is also a lipid

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83
Q

What is dislipidemia?

A

DLD is a broad term for abnormal lipid levels (can be high or low)

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84
Q

What are symptoms of elevated cholesterol?

A

typically not many symptoms arise until it develops into a disease or causes a stroke that you realize its a problem. Why lipid panels should be done annually

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85
Q

What are LDLs

A

Low-density lipoproteins; contain the most cholesterol Synthesized in the liver and transported to the tissues for building of plasma membranes and steroids Contributes to plaque deposits “BAD” cholesterol

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86
Q

What are HDLs?

A

High-density lipoprotein; transports cholesterol away from the body and back to the liver where it is used to make bile and excreted in the stool “GOOD” Cholesterol

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87
Q

What are VLDLs?

A

Very low density lipoproteins that carry triglycerides throughout the blood; reduces in size to LDL

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88
Q

What are lifestyle changes that can lower cholesterol?

A

Increase physical activity (30 min/5days/week) Maintain normal weight Reduce dietary saturated fat, trans fat, cholesterol Increase fiber (whole grains, vegetables, fruits) Eliminate tobacco use Will try lifestyle changes before medications and during if medications are indicated

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89
Q

Goal for cholesterol therapy?

A

Goals are no longer clear cut (treating the number) Now, take into account risk factors (age, smoking, family history, comorbidities)

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90
Q

Should those over 75 still take statins?

A

Insufficient evidence to recommend statin use when over 75. could cause higher risks by staying on the medication.

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91
Q

What are statins?

A

HMG-CoA Reductase Inhibitors Atrovastatin (Lipitor) Fluvastatin (Lescol) Lovastatin (Mevacor) Pravastatin (Pravachol) Simvastatin (Zocar)

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92
Q

What is the MOA of statins?

A

Limit cholesterol biosynthesis by inhibiting HMG-CoA which is needed for cholesterol production Lowers LDL; may also increase HDL and decrease triglycerides

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93
Q

What are the indications for statins?

A

First line treatment for hyperlipidemia (significant reduction in morbidity and mortality)

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94
Q

What are adverse effects of statins?

A

Myalgia (muscle aches/pains) - should ALWAYS be followed up on Diarrhea Increase glucose levels (risk increases in diabetic patients) Rhabdomyolysis (breakdown of muscle cells, will produce myalgia) Liver failure (rare) Eye lens opacities

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95
Q

Nursing implications for statins?

A
  • Check fasting lipid profile and liver function tests before starting therapy
  • Generally administered in the evening (hepatic cholesterol production increases at night) to make it more beneficial
  • Avoid taking with grapefruit juice (leads to toxicity by slowing down metabolism of drug)
  • Educate patients to report unexplained muscle pain, weakness, tenderness
  • Used in conjunction with diet and exercise
  • Onset 2 weeks
  • Maximum effects 4-8 weeks
  • Excess alcohol use increases risk for liver damage
  • Pregnancy category X
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96
Q

Bile Acid Sequestrants

A

Example: cholestyramine (Questran)

  • Bind bile acids (made from cholesterol) in intestine, preventing them from being recycled by the liver and re-entering circulation
  • Lowers LDL
  • Administered as a powder for suspension
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97
Q

Adverse effects of bile acid sequestrants

A
  • GI related side effects: abdominal pain, flatulence, conspitation, N/V, dyspepsia (upset stomach), steatorrhea (fatty stool), diarrhea
  • Do not take with other medications - it affects absorption
    • Take 2 hours before or 4 hours after
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98
Q

MOA of Niacin (Vitamin B3)

A
  • Not well understood
  • Decreases VDL (very effective), LDL, and triglycerides
  • Increases HDL
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99
Q

Implications for Niacin (Vitamin B3)

A

Treatment of hyperlipidemia

Usually used iwht other lipid lowering agents

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100
Q

Adverse effects of Niacin (Vitamin B3)

A
  • Flushing (especially with immediate release formulation)
  • GI distress (nausea, gas, diarrhea)
  • Abnormal liver function
    • Extended release is more toxic
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101
Q

Nursing implications of Niacin (Vitamin B3)

A
  • Educate patients regarind flushing to increase compliance
    • Aspirin helps to relieve this effect if taken 30 min before (only take if prescribed it anyway)
  • Take with cold water to help minimize flushing
  • Take on a full stomach
  • Different than what comes as a vitamin supplement; typically a significantly larger dose
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102
Q

Examples of Fibric Acid Derivatives

A
  • Have “fibr” in their name
  • femfibrozil (Lopid)
  • fenobribrate

Largely have replaced statins

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103
Q

MOA of fibric acid derivatives

A
  • Not well understood
  • Decrease triglycerides (very effective), VLDL
  • Increases HDL
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104
Q

Indicatin of fibric acid derivatives

A

Hypertriglyceridemia to decrease risk of CAD

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105
Q

Adverse effects of fibric acid derivatives

A
  • Abdominal pain
  • Nausea
  • Myalgia (muscle pain)
  • Abnormal liver function
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106
Q

What do cholesterol absorption inhibitors do?

A
  • Inhibit the absorption of cholesterol in the small intestine
  • Used in combination with a statin to lower LDL, or alone for familial hypercholesterolemia
  • Example: ezetimibe (Zetia)
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107
Q

Omega-3 fatty acids

A
  • Dietary supplement derived from marine and plant sources
  • Decrease triglycerides
  • Prophylaxis to prevent MI (unlabeled use)
    • No strong evidence
  • High doses can increase clotting time
    • Monitor, especially if they are on an anticoagulant
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108
Q

What are diuretics?

A

Something that increases urinary excretion of water

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109
Q

Common indication of diuretics?

A
  • Hypertension due to high volume of blood
  • Heart failure: lower volume heart needs to pump
  • Renal failure: excess fluid
  • Liver failure.cirrhosis: tends to collect extra fluid
  • Pulmonary edema: alveoli filled with fluid
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110
Q

What is a common concern when taking diuretics?

A

There effects on serum electrolytes, in particular, potassium (and magnessium)

High or low potassium levels cause heart problems

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111
Q

Therapeutic class of furosemide (Lasix)

A

Drug for heart failure, hypertension

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112
Q

Pharmacologic class of furosemide (Lasix)

A

Loop diuretic

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113
Q

Indications of furosemide (Lasix)

A

Heart failure, renal failure, hepatic cirrhosis, pulmonary edema, edema, HTN

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114
Q

MOA of furosemide (Lasix)

A

Inhibits reabsorption of sodium and chloride in the ascending loop of Henle

Results in increased excretion of sodium, potassium, chloride, calcium, magnessium, and water

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115
Q

Adverse effects of furosemide (Lasix)

A
  • Dehydration
  • Hypotension (low BP)
  • Dizziness
  • Electrolyte depletion (especially K+ and Mg+)
  • Renal impairment
    • Ototoxicity (higher doses, rapid IV administration
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116
Q

Nursing implications of furosemide (Lasix)

A
  • Monitor urine output, BP, creatinine, K+, Mg (may require electrolyte replacement)
  • May be on potassium supplement
  • Avoid taking at bedtime - fall risk
  • Educate patients on importance of monitoring lab work and BP
  • Rise slowly when getting up (orthostasis)
  • Related to sulfonamides - watch for cross-sensitivity (will still though)
  • Avoid using with other nephrotic or ototoxic (hearing) drugs
    • If taking digoxin, monitor for toxicity if hypokalemic (low potassium level)
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117
Q

Therapeutic class of hydrochlorothiazide (Microzide)

A

Antihypertensive, drug for edema

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118
Q

Pharmacologic class of hydrochlorothiazide (Microzide)

A

Thiazide diuretic

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119
Q

Indications for hydrochlorothiazide (Microzide)

A

Mild to moderate HRN (first-line drug), edema

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120
Q

MOA of hydrochlorothiazide (Microzide)

A

Affects sodium reabsorption (decreases) at the distal renal tubule, causing increased excretion of sodium and chloride

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121
Q

Adverse effects of hydrochlorothiazide (Microzide)

A
  • Electrolyte imbalances (decreased potassium, sodium, magnesium)
  • Hypotension
  • Vertigo
  • Renal impairment
    • Hyperglycemia in diabetic patients
122
Q

Nursing implications for hydrochlorothiazide (Microzide)

A
  • Monitor BP, urine output, electrolytes, renal function, administer in the morning
  • Less effective than loop diuretics (mild diuretic)
  • Examples: chlorothiazise (Diuril), hydrocholorthiazide (HCTZ)
123
Q

Therapeutic class of spironolactone (Aldactone)

A

Antihypertensive, drug for edema

124
Q

Pharmacologic class of spironolactone (Aldactone)

A

Aldoesterone antagonist

125
Q

Indications of spironolactone (Aldactone)

A
  • Heart failure
  • Edema with liver failure
  • HTN
  • Hyperaldosteronism (making too much aldosterone)
126
Q

MOA of spironolactone (Aldactone)

A

Inhibits aldoesterone, increasing the secretion of water and sodium, while decreasing the excretion of potassium

127
Q

Adverse effects of spironolactone (Aldactone)

A
  • Hyperkalemia
  • Hypoatrremia
  • Diarrhea
  • Gynecomastia (enlarged breasts)
128
Q

Nurisng implications of spironolactone (Aldactone)

A
  • Monitor urine output, BP, potassium levels
  • Educate clients to avoid eating foods high in potassium or salt substitutes high in potassium
129
Q

What is aldosterone?

A

A hormone produced by the adrenals that causes the kidneys to excrete potassium into the urine ad retain sodium in the renal tubulue (and therefore water)

Concentrates urine

130
Q

Carbonic anhydrase inhibitors

A
  • Indications: edema, glaucoma, epilepsy
  • Weak diruetic effect
  • Don’t use with sulfa-allergies
  • Example: acetazolamide (Diamox)
131
Q

Osmotic diuretic

A
  • Can be used IV
  • Indications: acute renal failure, closed-angle glaucoma, cerebral edema
  • Rarley used to toxicity
  • Highly potent
  • Example: mannitol
132
Q

What is cardiovascular disease?

A
  • Disorder of the heart and blood vessels
  • Includes:
    • Coronary artery disease
    • Heart failure
    • Cerebrovascular disease
    • Hypertension
    • Arrhythmias
    • Peripheral arterial disease
    • Congenital heart disease
    • Heart valve problems
    • Venous thromboembolism
  • # 1 cause of death globally
  • many can be prevented by modifying risk factors
133
Q

What is hypertension?

A

Elevation in arterial blood pressure

Systolic > 140

Diastolic > 90

Known as the silent killer

134
Q

What can hypertension lead to?

A
  • Cerebrovascular accident (stroke)
  • Myocardial infarction (heart attack)
  • Heart failure
  • Renal damage
  • Vision loss
135
Q

What influences blood pressure?

A
  • Blood volume
    • More blood volume, higher BP
  • Peripheral resistance/diameter of arterioles
    • Constriction of vessels, increased BP
  • Cardiac output
    • Increased output, increased BP
136
Q

What are mechanisms for controlling blood pressure?

A

The three influences of BP are controlled by baroreflexes and the renin-angiotensin-aldosterone system (RAAS)

137
Q

What are baroreflexes?

A

Baroreceptors located in the aortic arch and carotid sinuses sense a decrease in BP and respond by decreasing parasympathetic nervous system stimulation

The sympathetic nervous system responds by increasing vascular tone and cardiac output

138
Q

What is the RAAS system?

A
  • The kindeys sense a decrease in BP or decrease in sodium in the renal tubules and responds by releasing renin
  • Renin converts angiotensinogen to antiotensin I
  • Antiotensin-converting enzyme (ACE) then converts angiotension I to antiotensin II, which is a potent vasoconstrictor
  • Antiotensin II also stimulates the release of aldosterone (from the adrenal glands) which causes sodium reabsorption (leading to increased blood volume)
139
Q

First line treatments for HTN

A
  • Thiazide diuretics
  • Calcium channel blockers (CCB)
  • Angiotensin converting enzyme inhibitors (ACEI)
  • Angiotension receptor blockers (ARB)

African American population includes thiazides and CCBs, as they have a poorer response to ACEI and ARBs

140
Q

What do ACEI do?

A

Reduce BP by inhibiting the RAAS (dilating arteries and decreasing blood volume)

Excellent choice for diabetics as ACE Inhibitors slow the progression of kidney failure

Been shown to prevent death in people with heart failure after MI

Ends in -pril

141
Q

Therapeutic class of lisinopril (Prinivil, Zestril)

A

Drug for HTN, heart failure, MI prevention

142
Q

Pharmacologic class of lisinopril (Prinivil, Zestril)

A

ACE inhibitor

143
Q

Indications of lisinopril (Prinivil, Zestril)

A

HTN, heart failure, acute MI

144
Q

MOA of lisinopril (Prinivil, Zestril)

A

Prevents conversion of antiotension I to angiotension II; decreases vasoconstriction and aldoesterone secretion

145
Q

Adverse effects of lisinopril (Prinivil, Zestril)

A
  • Orthostatic hypotension
  • Dizziness
  • Headache
  • Peristent dry cough
  • Renal impairment
  • Hyperkalemia
  • Angioedema
146
Q

Nursing considerations for lisinopril (Prinivil, Zestril)

A
  • Discontinue if pregnant or planning pregnancy (toxic to fetus)
  • Patient education (signs of hypotension, angioedema, avoid high sodium and high potassiu foods, first dose phenomenon)
  • Monitor potassium and renal function (creatinine)
147
Q

What do angiotensin receptor blockers do?

A
  • Block the binding of angiotension II to angiotension receptors
  • Similar MOA and ACE inhibitors
  • Similar adverse effects (less incidence of cough and angioedema)
  • Good alternative to ACEI
  • Examples: candesartan, irbesartanm losartan, valsartan
148
Q

What do calcium channel blockers do?

A
  • Inhibit the entry of calcium into the cell, inhibiting muscle contraction (which leads to relaxation of arteriolar vasculature and a reduction in blood pressure)
  • Not typically chosen first for HTN nor used as monotherapy
  • African Americans tend to respond more favorably to CCBs
  • Three different subclasses that differ in their ability to treat HTN, angina, and arrhythmias
  • Examples: diltiazem, amlodipine, felodipine, nicardipine, nifedipine, verapamil
149
Q

Therapeutic class of diltiazem (Cardizem)

A

Antihypertensive, antianginal, antiarrhythmic

150
Q

Pharmacologic class for diltiazem (Cardizem)

A

Calcium channel blocker (CCB)

151
Q

Indications of diltiazem (Cardizem)

A

HTN, angina, tachyarrhythmias

152
Q

MOA of diltiazem (Cardizem)

A

Blocks transport of calcium into myocardial and vascular smooth muscle cells; inhibits muscle contraction (leads to relaxation of arteriolar vasculature and a reduction in blood pressure)

153
Q

Contraindications of diltiazem (Cardizem)

A

Heart block, shock

154
Q

Adverse effects of diltiazem (Cardizem)

A
  • Hyptension
  • Bradycardia
  • Heart failure symptoms
  • Headache
  • Fatigue
  • N/V
  • Arrhythmias
155
Q

Nursing considerations of diltiazem (Cardizem)

A
  • Monitor BP, HR, EKG (prior to and during therapy)
  • Can be given PO or IV
  • Do not crush extended release tablets
  • Patient education
156
Q

What are some second line treatments for HTN?

A
  • Additional therapies (not monotherapy)
  • Work on sympathetic nervous system (adrenergic receptors)
    • Beta adrenergic blockers (antagonists)
    • Alpha1 adrenergic blockers (antagonists)
    • Alpha2 adrenergic agonists
  • Work on the RAAS pathway
    • Aldosterone antagonists
    • Renin inhibitors
    • Direct vasodilators
157
Q

Indications for beta blockers (beta adrenergic antagonists)

A
  • HTN
  • Heart failure
  • Arrhythmias
  • Myocardial infarction
  • Many non-cardiovascular uses as well
158
Q

MOA for beta blockers

A

Block beta receptor site causes decreased HR and myocardial contractility; which in turn decreases BP and myocardial oxygen demand

159
Q

Adverse effects of beta blockers

A
  • Bradycardia
  • Hypotension
  • Dizziness
  • Fatigue/lethargy
  • Decreased sexual ability
  • Depression
  • Worsening of heart failure symptoms
  • Bronchoconstriction
160
Q

Nursing implications for beta blockers

A
  • Monitor BP and HR
  • Do not stop medication abruptly
  • May mask symptoms of hypoglycemia
  • Have patient report dizziness, lightheadedness
  • Avoid (or use with caution) in patients with asthma
161
Q

Selective vs non-selective beta blockers

A
  • Nonselective beta blockers block both B1 and B2 receptors
  • Selective beta blockers only block B1 receptors (cardioselective)
    • May lose this feature in high doses
162
Q

Indications for alpha1 adrenergic blockers

A

HTN, benign prostatic hypertrophy (BPH)

163
Q

MOA of alpha1 adrenergic blockers

A

Blocking the alpha1 adrenergic receptor results in vasodilation, and relaxation of smooth muscles inthe prostate

164
Q

Adverse effects of alpha1 adrenergic blockers

A
  • Orthostatic hypotension
  • Dizziness/drowsiness
  • Headache
  • Fatigue
  • Syncope
  • First dose phenomenon
165
Q

Nursing implications of alpha1 adrenergic blockers

A

Take at night to avoid dizziness/drowsiness, rise slowly when getting up

166
Q

Examples of alpha1 adrenergic blockers

A

doxazosin, prazosin, terazosin

167
Q

Indication of alpha2 adrenergic agonists

168
Q

MOA of alpha2 adrenergic agonists

A

Stimulate alpha2 adrenergic receptors causing decreased sympathetic response from the CNS (decreased vasodilation, and decreased BP)

169
Q

Adverse effects of alpha2 adrenergic agonists

A
  • CNS depression
  • Dizziness/drowsiness
  • Orthostatic hypotension
170
Q

Nursing implications of alpha2 adrenergic agonists

A
  • Do not stop abruptly (rebound HTN, withdrawal symptoms)
  • Rotate patch site each week
171
Q

What do vasodilators cause?

A

Directly causes relaxation of arteriolar smooth muscle, lowering blood pressure

Not a first line medication

172
Q

Adverse effects of vasodilators

A
  • Reflex tachycardia (compensation for decreased BP) which could preciptiate angina, MI, or heart failre
  • Sodium and water retention
  • These effects can be minimized by concomitant use of a diuretic and beta blocker
  • Flushing
  • Headache
  • N/V
  • Cyanide and thiocyanate toxicity
173
Q

MOA of vasodilators

A

Relaxation of venous and arterial smooth muscle, leading to vasodiltion and decreased peripheral resistance

174
Q

Nursing implications for vasodilators

A
  • Administered as IV continuous infusion
  • Rapid onset and short half-life (2 min)
  • Monitor BP, HR (do not decrease BP too quickly
  • Monitor for cyanide/thiocyanate toxicity (with high doses and/or prolonged therapy)
  • Transition to oral therapy ASAP
175
Q

What is heart failure?

A

When the heart is unable to pump enough blood and oxygen to adequately support other organs in the body (lack of perfusion; blood begins to back up)

Chronic, progressive disease

176
Q

Right side vs left side heart failure

A
  • Left pumps blood to the rest of the body, when it fails:
    • Blood backs up into the lungs
    • Shortness of breath, tripoding
  • Right pumps blood to the lungs, when it fails:
    • Blood backs up to the rest of the body (edema)
177
Q

Systolic vs diastolic heart failure

A
  • Diastolic heart failure (filling problem): not able to bring in blood; not able to relax
    • The inability of the left ventricle to relax normally, resulting in fluid backing up into the lungs
    • Diastolic heart failure leads to problems with heart relaxation and filling with blood
  • Systolic heart failure (pumping problem): can’t eject enough blood
    • The inability of the heart to contract enough to provide blood flow foward
    • Caues problems with contractions and ejection of blood
178
Q

Common causes of Heart failure

A
  • Coronary artery disease
  • Myocardial infarction
  • HTN
  • Diabetes
  • Arrhythmias
  • Valvular heart disease
  • Congenital heart disease
179
Q

Preload vs. afterload

A
  • Preload = stretch
    • Degree of ventricular stretch before contraction
    • Directly affected by blood volume in ventricles at end-diastole
    • Want a lower preload in HF, but not too low
  • Afterload = resistance
    • Resistance ventricles must overcome during systole
    • Directly affected by aortic tone/pressure
    • People in HF want low afterload
180
Q

What do inotropic drugs do?

A
  • Affect contractility
  • Positive inotropes increase the force of contractility
  • Negative inotropes decrease the force of contractility
181
Q

What do chronotropic drugs do?

A
  • Affect the heart rate
  • Positive chronotropes increase the heart rate
  • Negative chronotropes decrease the heart rate
182
Q

What is cardiac (ventricular) remodeling?

A

As blood backs up in the left ventricle, it enlarges and attempts to work harder to compensate for the increased blood volume. This changes the size, shape, and structure of the heart overtime as myocytes (cardiac cells) are injured and die. Cardiac tissue becomes fibrotic and fucntion decreases

183
Q

Lifestyle changes for Heart Failure?

A
  • Tobacco cessation
  • Salt restriction
  • Fluid restriction
  • Limit alcohol
  • Aerobic excercise (under medical supervision)
  • Stress managment
184
Q

Pharmacologic therapy for heart failure includes:

A
  • Reducing preload
  • Reducing blood pressure (reducing afterload)
  • Inhibit RAAs stimulation of sympathetic nervous system (decrease the stimulation of the sympathetic nervous system)

First line drugs:

  • ACE inhibitors
  • Diuretics
185
Q

How do ACE Inhibitors help heart failure?

A
  • Decrease afterload by decreasing peripheral reistance and BP
  • Decrease preload by vasodilation and inhibition of aldoesterone (causing diuresis and decreased blood volume)
  • Cardioprotectie effect - can stop or slow remodeling of the heart
  • Increase survival, improves symptoms, and decreases hospitalization
186
Q

How do diuretics help with heart failure?

A
  • Decrease preload by lowering blood volume through increased urine output
    • Decreases stretch on the heart and then it does not have to work as hard
  • Commonly used in conjunction with ACEI
187
Q

Second line drugs for heart failure

A
  • Cardiac glycoside
  • Beta blocker
  • Vasodilators
  • Phosphodiesterase inhibitors
  • Typically a combination of drugs are used
188
Q

Therapeutic class of digoxin (Lanoxin)

A

Drug for heart failure

189
Q

Pharmacologic class of digoxin (Lanoxin)

A

Cardiac glycoside

190
Q

Indications of digoxin (Lanoxin)

A

Heart failure, atrial fibrillation, atrial flutter

191
Q

MOA of digoxin (Lanoxin)

A

Increases intracellular calcium leading to positive inotropic effect (contractility). Decreases conduction through SA and AV nodes, leading to negative chronotropic effect (HR) and increased diastolic filling time (more time to perfuse)

192
Q

Adverse effects of digoxin (Lanoxin)

A
  • Bradycardia
  • Arrhythmias
  • Fatigue
  • N/V
  • Blurred/yellow vision (sign of toxicity)
  • Increased risk of toxicity when hypokalemic
193
Q

Nursing considerations of digoxin (Lanoxin)

A
  • Loading dose, followed by a daily maintenance dose (IV or PO)
  • Monitor drug levels (narrow therapeutic range)
  • Check apical pulse for one minute before administering (generally hold if HR <60)
  • Antidote is digoxin immune fab (Digibind)
  • Monitor potassium level
  • Many drug-drug interactions
  • very long half-life
194
Q

Beta blockers and heart failure

A
  • Block the effects of the sympathetic nervous system on the heart, decreasing the heart rate and BP (decreasing the workload of the heart)
  • Negative inotropic effect, important to monitor for worsening HF
  • Start low and slow
  • Typically combined with ACEI
  • Shown to decrease number of hospitalizations and deaths associated with HF
195
Q

Therapeutic class of carvedilol (Coreg)

A

Antihypertensive, drug for heart failure

196
Q

Pharmacologic class of carvedilol (Coreg)

A

Beta blocker

197
Q

Indications for carvedilol (Coreg)

A

HTN, heart failure, MI

198
Q

MOA of carvedilol (Coreg)

A

Block stimulation of Beta1, Beta2, and Alpha1 adrenergic receptors, leading to decreased heart rate and BP

199
Q

Adverse effects of carvedilol (Coreg)

A
  • Dizziness
  • Fatigue
  • Depression
  • Bradycardia
  • Weakness
  • Erectile dysfunction
  • Heart failure
  • Bronchospasm/wheezing
  • Diarrhea
  • Hyperglycemia
200
Q

Nursing considerations for carvedilol (Coreg)

A
  • Monitor BP, HR, weight, signs of worsening HF, glucose levels
  • Use with caution in patients with asthma
  • Client education: do not stop medication abruptly, monitor BP and HR, change position slowly, monitor weight for fluid retention
201
Q

Commonly used vasodilators for Heart failure

A
  • Hydralazine (Apresoline)
  • Isosobide dinitrate (Isordil)
202
Q

Therapeutic class of hydralizine (apresoline)

A

Antihypertensive

203
Q

Pharmacologic class of hydralizine (apresoline)

A

Vasodilator

204
Q

Indications of hydralizine (apresoline)

A

HTN, heart failure unresponsive to other therapies (off-label)

205
Q

MOA of hydralizine (apresoline)

A

Arteriolar vasodilation leading to decreased BP and afterload

206
Q

Adverse effects of hydralizine (apresoline)

A
  • Headache
  • N/V
  • Reflex tachycardia
  • Lupus-like symptoms (with higher doses or taking for long periods of time; rare)
    • Fever
    • Arthralgia
    • Myalgia
    • Malaise
    • Edema
    • Facial rash
207
Q

Nursing considerations of hydralizine (apresoline)

A
  • Monitor BP
  • Educate patient to notify provider if lupus-like symptoms develop
  • Take 3-4 times daily can lead to compliance issues
208
Q

Therapeutic class of milrinone (Primacor)

209
Q

Pharmacologic class of milrinone (Primacor)

A

Phosphodiesterase inhibitor

210
Q

Indications of milrinone (Primacor)

A

Acute, decompensated heart failure (short term therapy)

211
Q

MOA of milrinone (Primacor)

A

Blocking of phosphodiesterase enzyme leads to increased cardiac contractility (positive inotropic effect) and vasodilation (decreased preload and afterload).

This leads to increased cardiac output

212
Q

Adverse effects of milrinone (Primacor)

A
  • Hypotension
  • Arrhythmias
  • Angina
213
Q

Nursing implications of milrinone (Primacor)

A
  • Administered as a continuous IV infusion; short half-life
  • Monitor BP, cardiac output/index, EKG
214
Q

What are Human B-Type Natriuretic Peptides (BNP)

A
  • Secreted by ventricles in response to fluid overlad
  • Caues natriuretic effect (increases sodium excretion) and inhibits the RAAS system (vasodilation)
  • Nesiritide (Natrecor) is a vasodiltor identical to BNP and is used for acute decompensated heart failure
  • Hypotension is a common adverse effect; do not administer if SBP < 90
215
Q

What is angina? What are the types?

A
  • 3 types of angina (chest pain from lack of oxygen to heart)
    • Stable angina: fairly predictable as to frequency, intensity, and duration (typically relieved with rest)
    • Unstable angina: frquency arises more frequently, becomes more intense, or occurs during periods of rest
    • Variant (Prinzmetal’s) angina: occurs when decreased myocardial blood flow is caused by spasms of the coronary arteries
216
Q

Nonpharmacologic managment of angina

A
  • Lifestyle changes:
    • Limit alcohol
    • Low fat/cholesterol/sodoim diet
    • Manage cholesterol levels
    • Tobacco cessation
    • Maintin normal BP
    • Regular exercise
    • Weight management
    • Maintian normal glucose levels
    • Reduce stress
217
Q

Goals of pharmacologic management of Angina

A
  • Reduce intensity and frequency of episodes
  • Improve exercise tolerance
  • Increase tolerance for ADLs
  • Prevent consequences of ischemic heart disease
  • Prevent long term consequences
218
Q

What is the action of medications for angina?

A

Terminate an episode or decrease the frequency of episodes by decreasing myocardial oxygen demand:

  • Slow HR (beta blockers, calcium channel blockers)
  • Dilate veins (decrease preload)
  • Decrease contractility (negative inotrope - beta blockers, calcium channel blockers)
  • Decrease BP (decrease afterload)
219
Q

What are the drug categories used in angina? What is their purpose?

A
  • Organic nitrates
    • Rapid acting - terminate episode
    • Long acting - reduce frequency
  • Beta-adrenergic antagonists (beta blockers)
    • Reduce frequency (first line)
  • Calcium channel blockers
    • Reduce frequency (when BB not tolerate)
220
Q

What do nitrates do?

A
  • Relax both arterial and venous smooth muscle, reducing workload of the heart; dilate coronary arteries (works better on venous system)
  • Tolerance is rapidly gained and lost
  • Light degrades the product
  • Medications: isosorbide and nitroglycerin are both available in short and long acting formulas
  • Adverse effects: hypotension, dizziness, headache, flushing of the face, reflex tachycardia, development of tolerance
221
Q

Therapeutic class of: nitroglycerin (Nitrostat, Nitro-Bid, Nitro-Dur, others)

A

Antianginal drug

222
Q

Pharmacologic class of nitroglycerin (Nitrostat, Nitro-Bid, Nitro-Dur, others)

A

Organic nitrate, vasodilator

223
Q

Actions and uses of nitroglycerin (Nitrostat, Nitro-Bid, Nitro-Dur, others):

A
  • relaxes arterial and venous (works better on venous) smooth muscles; reduces workload of the heart; dilate coronary arteries
  • Taken during acute episode or prior to physical activity
224
Q

Adverse effects of nitroglycerin (Nitrostat, Nitro-Bid, Nitro-Dur, others)

A
  • Usually cardiovascular in nature and rarely life threatening
  • Headache due to dilation of cerebral vessels
  • Reflex tacchycardia due to venous dilation
    • May prescribe beta blockers to diminish
225
Q

Nursing Implications of nitroglycerin (Nitrostat, Nitro-Bid, Nitro-Dur, others)

A

If no relief after 3rd dose, sign of MI

Needs special bottle and IV so plastic does not absorb the medication; sensitive to light

226
Q

Interactions with nitroglycerin (Nitrostat, Nitro-Bid, Nitro-Dur, others)

A

Concurrent use with phosphodiesterase-5 inhibitors, such as sildenafil (Viagra), vardenafil (Levitra), or tadalafil (Cialis), can cause life-threatening hypotension and cardiovascular collapse; use with alcohol and antihypertensive drugs may cause addtive hypotension

227
Q

Beta blockers and angina

A
  • Reduce the cardiac workload by slowing heart rate and reducing contractility
    • Negative inotrope and chronotrope
  • Used for angina prophylaxis
  • Adverse effects: bradycardia, hypotension, dizziness, fatigue/lethargy, decreased sexual ability, depression, worsening heart failure symptoms, bronchoconstriction
  • Patient Teaching
    • Rise slowly - orthostatic hypertension
    • Do not suddenly stop taking - sudden cessation can cause angina
    • Check pulse daily and report < 60
    • Check BP daily and report <90/60
    • Report depression/fatigue - contact provider if this is occurring
228
Q

Therapeutic class of atenolol (Tenormin)

A

Antianginal drug

229
Q

Pharmacologic class of atenolol (Tenormin)

A

Beta-adrenergic blocker

230
Q

Actions and uses of atenolol (Tenormin)

A
  • Selective beta1-adrenergic receptor on the heart
    • Slows heart rate and reduces contractility (lowers myocardial ocygen demand)
231
Q

Indications of atenolol (Tenormin)

A

Chronic disorders: HF, HTN, angina, and MI

232
Q

Adverse effects of atenolol (Tenormin)

A
  • Few adverse effects on the lungs
  • Fatigue, weakness, bradycardia, and hypotension
  • Do not discontinue abruptly
233
Q

Calcium channel blockers and angina

A
  • Used if patient is not tolerating beta blockers
  • Inhibits transport of calcium into myocardial cells, relaxing arteriolar smooth muscle (decreasing workload on the heart), dilate coronary arteries
  • Reduce myocardial oxygen demand by lowering BP and HR (different classes variy in their ability to affect HR)
  • Adverse effects: hypotension, bradycardia, heart failure symptoms, headache, fatigue, arrhythmias
234
Q

What is an infarction

A

Some tissues have died due to lack of oxygen/blood flow

235
Q

What is necrosis

A

Cell death

236
Q

What is coronary circulation?

A

Small arteries and veins that help supply the heart with bloos and oxygen

When blocked - heart attach occurs

237
Q

Symptoms of MI

A
  • Chest pain/pressure - referred pain to left arm/jaw
  • Diaphoresis (sweating)
  • Nausea
  • Fatigue
  • Dyspnea
238
Q

Lab tests for MI

A
  • Troponin I
  • Troponin T
  • CK-MB
239
Q

Complications of MI

A
  • Arrhythmias
  • Cardiogenic shock
  • Pericarditis
  • Myocardial rupture
  • Heart failure
240
Q

What is reperfusion injury?

A

Tissue damage by returning blood to the heart.

Increased calcium flow causes muscle contraction that can have cells stuck in contraction.

Reactive oxygen species can cause damage

241
Q

What are medications for MI

A
  • Antiplatelets - aspirin
  • Anticoagulants - heparin
  • Nitrates - relax coronary arteries; lowers preload
  • Beta blockers - slow heart rate
  • Pain medication
  • Statins - improve lipid profile
242
Q

Goals of treating MI

A
  • Early diagnosis and treatment to reduce myocardial ischemia and damage, relieve pain, reduce mortality and long term disability
  • Restore blood supply (reprefusion) - PTCA, thrombolytics, or CABG
  • Reduce myocardial oxygen demand - nitrates, BB, CCB
  • Control/prevent dysrhhythmias - BB, other antidysrhythmics
  • Reduce post MI mortality - aspirin (ASA), BB, ACE inhibitors
  • Manage pain/anxiety - narcotic analgesia (morphine)
  • Prevent inlargment of clot - anticoagulants, antiplatelet drugs
243
Q

What are thrombolytics?

A
  • Dissolve clots obstructing coronary arteries to restore perfusion to myocardium; prevents all clots in body - do not give if trauma (especially brain bleed)
  • Administer within 12 hours after onset of symptoms
  • Narrow margin of safety
  • Side effects: hemorrhage, hypotension
  • Short half-life
  • Nursing considerations
    • Contraindications
    • Administered IV through dedicated line
    • Frequent vitals
    • Hourly neuro chekcs
    • Monitor for bleeds
    • Client on bed rest
    • EKG monitoring
    • Avoid invasive procedures
  • Examples: reteplase, alteplase (TPA), tenecteplase
244
Q

Beta blockers and MI

A

Reduce cardiac oxygen demand by slowing HR, decreasing contractility, and reducing BP

Helps suppress reperfusion dysrhythmias

Decreases mortality if given within 8 hours of MI

245
Q

What is hemostasis

A

The stopping of blood flow; it is a complex process that attempts to maintain balance between blood fluidity and coagulation

246
Q

The body’s removal of blood clots

A
  • Clots stop excessive bleeding but restrict blood flow to the affected area
  • To restore circulation to the tissues, clots are removed by fibrinolysis
  • Fibrinolysis starts 24-48 hours after clot formation and continues until clot is dissolved
  • Tissue plasminogen activator (tPA) is an enzme secreted by blood vessels located near the clot
    • TPA converts plasminogen to plasmin which digests fibrin strands, dissolving the clot
247
Q

Anticoagulants

A

Used to prevent formation of clots; incresae normal clotting time; used primarily to prevent formation in veins (fibrous clots)

Do not dissolve preexisting clots

248
Q

Antiplatelet agents

A

Inhibit platelet aggregation; primarily used to prevent clot formation in arteries (platelet clots)

249
Q

Thrombolytics

A
  • Dissolve life-threatening clots
  • Goal is to quickly restore bloodflow
  • Used in acture MI, pulmonary embolism, ischemia (CVA (stroke), DVT, arterial thrombosis, blocked IV catheter
    • Life or limb threatening situations
  • Converts plasminogen to plasmin which initiates fibrinolysis
  • Narrow margin of safety
  • Followed by anticoagulants or antiplatelet meds
  • Examples: reteplas, alteplase, tenecteplase
250
Q

Hemostatics

A

Promote formation of clots; inhibit normal remoal of fibrin; speed clot formation

251
Q

Therapeutic class of heparin

A

Anticoagulant

252
Q

Pharmacologic class of heparin

A

Indirect thrombin inhibitor

253
Q

Indications of heparin use

A

Prevent formation of clots

Prophylactically in hospitals

254
Q

MOA of heparin

A

The binding of heparin to antithrombin III blocks clotting through the inactivation of Factor X and inhibition of prothrombin’s conversion to thombin (thrombin inhibitor)

255
Q

Adverse effects of heparin

A
  • Bleeding
  • Heparin induced thrombocytopenia (HIT)
    • Increases risk for clotting and has low platelet stte
    • Auto-immune reaction
256
Q

Nursing implications for heparin

A
  • Administered SQ or IV (IV greater risk for HIT)
  • Monitor for bleeding
  • Monitor for platelets (HIT)
  • Monitor PTT (partial thromboplastin time)
  • May also monitor anti-Factor Xa levels
  • Protamine sulfate is antidote
  • Half life is about an hour (Can get off an go to surgery)
  • Black box warning: epidural or spinal hematomas may occur when heparin or LMWHs are used in patients receiving spinal anesthesia or lumbar puncture - can result in long-term or permanent paralysis, frequent neuro monitoring is essential
257
Q

Low Molecular Weight Heparins (LMWHs)

A
  • Enoxaparin (Lovenox)
  • Indications: prophylaxis and treatment of DVT and PE; unstable angina; non-Q-wave MI
  • MOA: binds to antithrombin and accelertes its ability to inhibit factor Xa, preventing the growth of thrombi
  • Adverse effects: bleeding, bruising at the injection site
  • Nursing implications:
    • Syringes come pre-made - do not expell the air bubble; helps to seal in the medication
    • Longer half life
    • No lab monitoring necessary
258
Q

Therapeutic class of warfarin (Coumadin)

A

Anticoagulant

259
Q

Pharmacologic class of warfarin (Coumadin)

A

Vitamin A antagonist

260
Q

Indications of warfarin (Coumadin)

A
  • Prevent formation of clots; can be used prophylactically
  • Mechanical heart valves
  • Arrhythmias
261
Q

MOA of warfarin (Coumadin)

A

Blocks the generation of vitamin K, thereby inhibiting the synthesis of vitamin K dependent clotting factors

Different parts of the vlotting cascade need vitamin K

262
Q

Adverse effects of warfarin (Coumadin)

A

Bleeding, skin necrosis (rare)

263
Q

Nursing implications of warfarin (Coumadin)

A
  • Given at the same time every day
  • Takes several doses to reach maximum effects (overlaps with heparin therapy)
    • No loading dose
  • Monitor Pt/INR
  • Educate clients about bleeding precautions
  • Cotnraindicated in pregnancy
  • Outpatient follow up and education
  • Leafy green vegetables are rich in vitamin K - can reduce the ability of anticoagulants to work
264
Q

Contraindications for Thrombolytics

A
  • Previous intracranial hemorrhage
  • Recent ischemic stroke (3 months)
  • Recent internal bleeding
  • Recent intracranial or spinal surgery
  • Recent major surgery, trauma, prolonged CPR
  • Intracranial neoplasm
  • Arteriovenous malformation or aneurysm
  • Suspected aortic dissection
  • Severe, uncontrolled hypertension
265
Q

Antifibrolytics

A

Action is opposite anticoagulants

Shortens bleeding time - enhances the stability of clots by preventing fibrin of dissolving

Used to prevent excessive bleeding after surgery or with people who have systemic clotting disorders

266
Q

Dysrhythmias

A
  • Abnormal impulse formation or conduction in the myocardium
  • Dysrythmias vary in severity from being completely asymptomatic to life-threatening
  • EKG required to diagnose
  • Can lead to stroke or heart failure
  • Symptoms are typically related to decrease in cardiac output
267
Q

Dysrhythmia symptoms

A

Decreased blood flow causes:

  • Low BP
  • Confusion
  • Dizziness
  • Chest pain
  • Shortness of breath
268
Q

Goal of antydysrhythmic drugs

A
  • To prevent it from coming back or terminating current dysrhythmia
  • They carry the potential to worsen or create new dysrhythmias
  • Reserved for symptomatic dysrhythmias
269
Q

Types of drugs for dysrhythmias

A

Sodium channel blockers

Beta adrenergic blockers

Potassium chennel blockers

Calcium channel blockers

Miscellaneous drugs

270
Q

Sodium channel blockers

A
  • Largest group of antidysrhythmic
  • Differentiated by speed of binding and dissociation from receptor sites
  • Chemical structure and action similar to local anesthetics
  • Frequent EKGs should be obtained
  • Examples: procainamide, lidocaine
271
Q

Beta adrenergic blockers

A
  • Slowing of heart rate and decreased conduction velocity through the AV node can suppress several types of dysrhythmias
  • Typically used for atrial dysrhythmias
  • Examples: propranolol, metoprolol (off-label)
  • Need to check BP before administration
272
Q

Potassium channel blockers

A

Prolongs the refractory period, which stabilizes dysrhythmias

Refractory period is the period of time when the cells are depolarized and cannot initiate another action potential

273
Q

Therapeutic class of amiodarone (Cordarone)

A

Antidysrhtymic

274
Q

Pharmacologic class of amiodarone (Cordarone)

A

potassium channel blocker

275
Q

Inidcations of amiodarone (Cordarone)

A

Treatment of lifethreatening ventricular dysrhythmias

Tratment of arterial dysrhythmias (off-label)

276
Q

MOA of amiodarone (Cordarone)

A

Prolongs action potential and refractory period, slowing the heart rate. Decreases peripheral vascular resistance through vasodilation (not so much orally as IV - watch BP)

277
Q

Adverse effects of amiodarone (Cordarone)

A
  • Worsening of dysrhythmias
  • Pulmonary toxicity (long-term scarring of lung tissue)
  • Brady cardia
  • Hypotension
  • N/V
  • Dizziness
  • Fatigue
  • Blue discoloration of the skin (long term; sun screen can help; typically goes away when drug is discontinued)
  • Increased liver enzymes
  • Effect on thryoid function
  • Photosensitivity
  • Tremors
  • Blurry vision
278
Q

Interactions of amiodarone (Cordarone)

A

Multiple drug interactions - increases drug levels of diogxin, warfarin, and carveilol

279
Q

Nursing considerations of amiodarone (Cordarone)

A
  • Requires a loading dose
  • EKG monitoring if given IV
  • Monitor HR and BP
  • Assess for signs of pulmonary toxicity (through respiratory assessment)
  • Monitor liver and thyroid function
  • Avoid grapefruit juice
  • Prolonged half-life
  • Pregnancy category D
280
Q

Calcium channel blocker

A

Stabilize dysrhythmias by decreasing automaticity at SA node, slowing conduction velocity through the AV node, and prolonging the refractory period

Generally well tolerated

Examples: verapamil, diltiazem

281
Q

A 62-year-old man is admitted to the cardiac intensive care unit. His heart rate is dangerously low at 32 beats/minute. Which of the following medications can be used for the treatment of bradycardia (low heart rate)?

a. Isoproterenol (a nonselective beta adrenergic antagonist)
b. Prazosin (an alpha1 adrenergic antagonist
c. Donepezil (a cholinesterase inhibitor)
d. Atropine (an anticholinergic)

A

d. Atropine (an anticholinergic)

282
Q

A nurse is to give phenylephrine (an alpha1 adrenergic agonist) parenterally. What safety precaution would be necessary, especially with this drug?

a. Monitor patency throughout the infusion
b. Monitor the client’s temperature every hour during the infusion
c. Monitor for CNS depression
d. Monitor for hypotension throughout the infusion

A

a. Monitor patency throughout the infusion

283
Q

A client taking bethanechol (Urecholine), a cholinergic medication, may experience which of the following adverse effects?

a. Tachycardia
b. Hypertension
c. Diarrhea
d. Urinary retention

A

c. Diarrhea

284
Q

Epinephrine is a nonselective adrenergic agonist. What is the disadvantage of this nonspecific action?

a. It causes more autonomic side effects
b. This drug cannot be used for nervous system conditions
c. It will not cross the blood-brain barrier
d. It can only be given by subcutaneous injection

A

a. It causes more autonomic side effects

285
Q

A client taking neostigmine (Prostigmin), a cholinesterase inhibitor, should be taught to observe for which of the following adverse effects that may signal a possible overdose?

a. Excessive sweating, salivation, and drooling
b. Extreme constipation
c. Hypertension and tachycardia
d. Excessively dry eyes and reddened sclera

A

d. Excessively dry eyes and reddened sclera

286
Q

A client is started on atenolol (Tenormin), a beta1 adrenergic blocker. Which is the most important action to be included in the plan of care for this patient related to this medication?

a. Monitor pulse and blood pressure
b. Mydriasis may cause blurred vision
c. Consume foods high in potassium
d. Monitor for urinary retention

A

a. Monitor pulse and blood pressure

287
Q

Which of the following is a loop diuretic?

a. Mannitol
b. Spironolactone
c. Furosemide
d. Hydrochlorothiazide

A

c. Furosemide

288
Q

Which is a potential adverse effect of taking spironolactone (Aldactone)?

a. Elevated sodium
b. Low glucose
c. Elevated potassium
d. Low potassium

A

c. Elevated potassium

289
Q

Milrinone (a phosphodiesterase inhibitor) directly produces which of the following effects?

a. Increased vasoconstriction and blood pressure
b. Increased urine output
c. Increased heart rate
d. Increased contractility and vasodilation

A

d. Increased contractility and vasodilation

290
Q

The purpose of a beta blocker as part of the treatment for heart failure is to:

a. Increase urine output
b. Lower cardiac workload by decreasing sympathetic stimulation
c. Increase the contractility of the heart muscle
d. Cause peripheral vasoconstriction

A

b. Lower cardiac workload by decreasing sympathetic stimulation

291
Q

Administering high dose IV furosemide too rapidly may cause the following adverse reaction?

a. Dangerously low serum potassium
b. Ototoxicity
c. Orthostatic hypotension
d. Bronchospasm

A

b. Ototoxicity

292
Q

Which commonly used heart failure medication has both alpha and beta antagonist properties?

a. Milrinne (Primacor)
b. Hydralazine (Apresoline)
c. Carvedilol (Coreg)
d. Lisinopril (Zestril)

A

c. Carvedilol (Coreg)

293
Q

Dobutamine is used in severe cases of heart failure to increase contractility. This is known as:

a. A positive contractatrope
b. A positive dromotrope
c. A positive chronotrope
d. A positive inotrope

A

d. A positive inotrope

294
Q

A sign for toxicity for this medication is blurred, yellow vision:

a. Digibind
b. Furosemide
c. Digoxin
d. Protamine

A

c. Digoxin

295
Q

For which class of anti-HTN drugs should the nurse consider giving the first dose at bedtime?

a. Alpha1 antagonists
b. Diuretics
c. Beta antagonists
d. Vasodilators

A

a. Alpha1 antagonists

296
Q

Which of the following is an angiotensin II receptor blocker (ARB)?

a. Captopril (Capoten)
b. Amlodipine (Norvasc)
c. Hydralazine (Apresoline)
d. Valsartan (Diovan)

A

d. Valsartan (Diovan)

297
Q

Which of the following medications is contraindicated in pregnancy?

a. Enalapril (Vasotec)
b. Lisinopril (Zestril)
c. Losartan (Cozaar)
d. All of the above

A

All of the above

298
Q

Which of the following classes of antihypertensive drugs can mask symptoms of hypoglycemia?

a. Alpha2 adrenergic agonists
b. Angiotensin converting enzyme inhibitors
c. Calcium channel blockers
d. Beta adrenergic antagonists

A

d. Beta adrenergic antagonists

299
Q

Which autonomic drug class is commonly used to dry the nasal mucosa?

a. Parasympathomimetics
b. Cholinergics
c. Sympathomimetics
d. Beta adrenergic blockers

A

c. Sympathomimetics

300
Q

Which of the following drug classes is not prescribed for asthma?

a. Beta2 agonists
b. Corticosteroids
c. Methylxanthines
d. Beta blockers

A

d. Beta blockers

301
Q

The use of leukotriene modifiers (montelukast/Singulair) in the treatment of asthma is to:

a. Stimulate bronchodilation and terminate an acute attack
b. Reduce coughing and secretions
c. Reduce inflammation and frequency of episodes
d. Thin mucous and prevent infection

A

c. Reduce inflammation and frequency of episodes

Pharmacology for Nurses (11 decks)

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