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Krystan: Semester Two Nursing School > 2820 Pharmacology Exam 2 > Flashcards

2820 Pharmacology Exam 2 Flashcards

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1
Q

Classes of sedative hypnotics

A

Benzodiazepines
Nonbenzodiazepines
Melatonin agonists
IV anesthetics

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2
Q

Classes/types of non-opioid analgesics

A

NSAIDs

Acetaminophen

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3
Q

Examples of adjuvant medications

A

Amitriptyline
Gabapentin
Hydroxyzine
Ibuprofen

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4
Q

Examples of miscellaneous pain medications

A

Sumatriptan
Erogtamine
Propranolol

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5
Q

Diazepam: class and category

A 
Sedative hypnotic (schedule IV)
Benzodiazepine
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6
Q

Diazepam: pharmacological action

A

Binds to GABA receptors to intensify effects of GABA, relaxing skeletal muscles

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7
Q

What does GABA do in the body?

A

Reduce neuronal excitability throughout the CNS

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8
Q

Diazepam: therapeutic uses

A 
Anxiety disorders
Preoperative sedation
Conscious sedation
Managing alcohol withdrawal
Muscle relaxation
Short term insomnia
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9
Q

Diazepam: evaluation of medication effectiveness

A

Decreased anxiety
Seizure control
Decreased muscle spasms
Decreased symptoms of alcohol withdrawal

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10
Q

Zolpidem: class and category

A

Nonbenzodiazepine sedative hypnotic (schedule IV)

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11
Q

Zolpidem: pharmacological action

A

binding at GABA sites to cause CNS depression (without the analgesic effect of benzodiazepines)

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12
Q

Zolpidem brand name

A

Ambien

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13
Q

Zolpidem: therapeutic use

A

Insomnia, especially with difficulties falling asleep

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14
Q

Zolpidem: evaluation of effectiveness

A

Relief from insomnia

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15
Q

What is a common melatonin agonist?

A

Ramelteon

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16
Q

What is the mechanism of action for NSAID’s?

A

Inhibition of prostaglandin synthesis (prostaglandins induce pain by free radical formation)

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17
Q

Why is aspirin not recommended for pain?

A

Doses need for pain management put patient at significant risk for bleeding

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18
Q

Ibuprofen: class

A

NSAID/non-opioid analgesic

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19
Q

Ibuprofen: pharmacological action

A

Inhibits prostaglandin synthesis

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20
Q

Ibuprofen: therapeutic use

A

Pain
Fever
Inflammatory disorders

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21
Q

Ibuprofen: evaluation of effectiveness

A

Decreased pain
Increased joint mobility
Fever reduction

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22
Q

Naproxen: class

A

NSAID/non-opioid analgesic

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23
Q

Naproxen: pharmacological action

A

Inhibits prostaglandin synthesis

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24
Q

Naproxen: therapeutic use

A 
Mild to moderate pain
Fever
Dysmenorrhea 
Inflammatory disorders
Osteoarthritis
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25
Q

Naproxen: evaluation of effectiveness

A

Reduced pain
Increased joint mobility
Fever reduction

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26
Q

Acetaminophen: class

A

Non-opioid analgesic

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27
Q

Acetaminophen: pharmacological action

A

Inhibits prostaglandin synthesis (without anti-inflammatory effects)

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28
Q

Acetaminophen: therapeutic use

A

Pain

Fever

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29
Q

Acetaminophen: evaluation of effectiveness

A

Pain and fever relief

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30
Q

What are some examples of opioid agonists?

A 
Morphine
Fentanyl
Merperidine
Codeine
Oxycodone
Hydromorphone
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31
Q

What is the gold standard medication for pain management?

A

Morphine

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32
Q

How do opioid agonists work in the body?

A

They bind to and activate mu and kappa receptors

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33
Q

Morphine: class

A

Opioid agonist

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34
Q

Morphine: pharmacological action

A

Bind to opiate receptors in CNS, altering pain perception and response while depressing CNS

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35
Q

Morphine: therapeutic use

A

Severe pain when other treatment options are inadequate
Pulmonary edema
MI pain

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36
Q

Morphine: evaluation of effectiveness

A

Decreased pain without altered LOC or respiratory status

Decreased symptoms of pulmonary edema

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37
Q

Fentanyl: class

A

Opioid agonist

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38
Q

Fentanyl: pharmacological action

A

Binds to opiate receptors in CNS, altering pain perception/response

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39
Q

Fentanyl: therapeutic use

A

Supplement to anesthesia

Induction and maintenance of anesthesia

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40
Q

Fentanyl: evaluation of effectiveness

A

Quiescence
Reduced motor activity
Analgesia

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41
Q

Oxycodone: class

A

Opioid agonist

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42
Q

Oxycodone: pharmacological action

A

Binding to opiate receptors in CNS

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43
Q

Oxycodone: therapeutic use

A

Moderate to severe pain requiring round the clock treatment

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44
Q

Oxycodone: evaluation of effectiveness

A

Decreased pain severity without altered level of consciousness or respiratory status

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45
Q

Naloxone: class

A

Opioid antagonist

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46
Q

Naloxone: pharmacological action

A

Competitively blocks opioid receptors to block effects of opioids

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47
Q

Naloxone: therapeutic use

A

Reversal of CNS depression because of opioid overdose

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48
Q

Naloxone: evaluation of effectiveness

A

Adequate ventilation following opioid excess

Alertness without pain or withdrawal symptoms

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49
Q

What should the nurse remember about administering naloxone?

A

It has a very short half life, so will need to be administered frequently for effectiveness (and administered until opioids are out of system)

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50
Q

Amitriptyline: class

A

Tricyclic Antidepressant

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51
Q

Amitriptyline: pharmacological action

A

Increases synaptic concentration of serotonin and norepinephrine (potentiates their effects)

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52
Q

Amitriptyline: therapeutic use

A

Depression
Anxiety
Also found to help with chronic pain syndromes and insomnia

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53
Q

Amitriptyline: evaluation of effectiveness

A

Increased sense of well-being
Renewed interest in surroundings
Improved appetite, energy level, and sleep
Decreased chronic pain

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54
Q

Gabapentin: class

A

Anticonvulsant/analgesic adjunct/mood stabilizer

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55
Q

Gabapentin: pharmacological action

A

Uncertain, but may inhibit excitatory neuron activity and affect amino acid transport

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56
Q

Gabapentin: therapeutic uses

A 
Partial seizures
Neuralgia
Restless leg syndrome
Neuropathic pain
Diabetic neuropathy 
Depression 
Anxiety
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57
Q

Gabapentin: evaluation of effectiveness

A 
Decreased seizure frequency
Decreased pain
Decreased migraines
Increased mood stability 
Decreased effects of restless leg syndrome
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58
Q

Sumatriptan: class

A

5HT1 agonist (vascular headache suppressant)

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59
Q

Sumatriptan: pharmacological action

A

Selective agonist of 5HT1 vascular serotonin receptor sites, causing vasoconstriction in large intracranial arteries

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60
Q

Sumatriptan: therapeutic use

A

Relief of acute migraine attack

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61
Q

Sumatriptan: evaluation of effectiveness

A

Migraine relief

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62
Q

What is the mechanism of action for beta 2 adrenergic agonists?

A

Activate SNS to relax bronchial smooth muscle, causing bronchodilation

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63
Q

What is a drawback to beta agonists?

A

No anti-inflammatory ability so they cannot help with asthma inflammation

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64
Q

What diseases are beta agonists used for primarily?

A

Asthma, COPD, and cystic fibrosis

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65
Q

What is the benefit of short acting beta agonists?

A

Rapid onset of action

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66
Q

What are short acting beta agonists (SABAs) prescribed for?

A

Preventing or terminating an asthma attack

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67
Q

SABAs are also known as

A

Rescue drugs or a rescue inhaler

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68
Q

How long do the effects of SABAs last?

A

2-6 hours

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69
Q

Albuterol: class

A

Beta 2 adrenergic agonist

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70
Q

Albuterol: pharmacological action

A

Bind to beta 2 adrenergic receptors in airway to decrease intracellular calcium and relax smooth muscle in the airway

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71
Q

Albuterol: therapeutic use

A

Treatment or prevention of bronchospasm in COPD or asthma

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72
Q

Albuterol: evaluation of effectiveness

A

Prevention or relief of bronchospasm

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73
Q

How long do the effects of long acting beta agonists (LABAs) last?

A

Up to 12 hours

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74
Q

Why do LABAs have a black box warning?

A

Increased risk of asthma related deaths, because effects are not immediate and patient is in trouble if they take them during an acute attack

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75
Q

What is the benefit of LABA’s?

A

Minimal systemic effects or toxicity

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76
Q

Salmeterol: class

A

Beta 2 adrenergic agonist

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77
Q

Salmeterol: pharmacological action

A

Causes accumulation of cAMP at beta 2 adrenergic receptors in the lungs to cause bronchodilation

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78
Q

Salmeterol: therapeutic use

A

Prevention of bronchospasm in patients with poorly controlled asthma
Prevention of exercise induced asthma

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79
Q

Salmeterol: evaluation of effectiveness

A

Prevention of exercise induced asthma

Prevention of bronchospam or reduced number of acute asthma attacks

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80
Q

What is the most common route of administration of beta agonists for respiratory conditions?

A

Inhalation

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81
Q

Why do inhaled beta agonists cause minimal systemic toxicity?

A

Only small amounts are absorbed into the body

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82
Q

What may happen with chronic use of beta agonists?

A

Tolerance can develop, leading to shorter duration of action

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83
Q

What does increased use of beta agonists over a period of hours or days indicate?

A

Rapidly deteriorating/poorly managed condition that needs medical intervention

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84
Q

What is the mechanism of action for anticholinergics?

A

Compete with ACh for binding at muscarinic receptors, blocking parasympathetic response (bronchodilation occurs)

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85
Q

Ipratropium: class

A

Anticholinergic

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86
Q

Ipratropium: pharmacological action

A

Inhibits cholinergic receptors in bronchial smooth muscle, leading to local bronchodilation

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87
Q

Ipratropium: therapeutic use

A

Maintenance therapy of reversible airway obstruction due to COPD

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88
Q

Ipratropium: evaluation of effectiveness

A

Decreased dyspnea
Improved breath sounds
Decreased rhinorrhea

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89
Q

Why is ipratropium the most frequently prescribed anticholinergic for COPD?

A

Slower onset of action with less intense bronchodilation than beta agonists

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90
Q

What is the first line treatment combination for COPD?

A

Ipratropium and albuterol

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91
Q

What is the benefit of combining ipratropium with a beta agonist?

A

Greater and more prolonged bronchodilation than either med can provide separately

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92
Q

What is the primary use for methylxanthines?

A

Long term management of persistent asthma that is unresponsive to beta agonists or corticosteroids

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93
Q

How do methylxanthines work?

A

They are chemically similar to caffeine, and relax muscles in airways

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94
Q

Why are methylxanthines infrequently prescribed?

A

Narrow safety margin, especially with prolonged use

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95
Q

What are two examples of methylxanthines?

A

Theophylline and aminophylline

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96
Q

What is the mechanism of action for corticosteroids?

A

Dampen activity of inflammatory cells and increase production of anti-inflammatory mediators

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97
Q

What is the effect of corticosteroids on bronchial smooth muscle?

A

They sensitize bronchial smooth muscle to respond to beta agonist stimulation (often used in conjunction)

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98
Q

What is the intended use of inhaled corticosteroids?

A

Preventing asthma attacks

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99
Q

When might a systemic corticosteroid be used to treat asthma?

A

Severe, unstable asthma that is unresponsive to other treatment. Intended for short term use only

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100
Q

What are the adverse effects of using using systemic corticosteroids for more than 10 days?

A

Adrenal gland suppression/atrophy
Peptic ulcers
Hyperglycemia
Growth retardation in children

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101
Q

Why can you not stop taking systemic corticosteroids abruptly?

A

Because corticosteroids suppress the adrenal gland and supply the body’s cortisol, and if discontinued suddenly, the adrenal glands won’t be able to meet the cortisol demands. Must be tapered off gradually

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102
Q

What can long term systemic corticosteroid use cause?

A

Cushing’s syndrome

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103
Q

Prednisone: class

A

Corticosteroid (systemic)

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104
Q

Prednisone: pharmacological action

A

Suppress inflammation and normal immune response

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105
Q

Prednisone: therapeutic use

A

Asthma

Other things unrelated to oxygenation

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106
Q

Prednisone: evaluation of effectiveness

A

Decrease in symptoms with minimal systemic effects

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107
Q

What are leukotrienes?

A

Bodily mediators of immune response involved in allergic and asthmatic reactions. They promote airway edema and inflammation

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108
Q

Montelukast: class

A

Leukotriene antagonist

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109
Q

Monteleukast: pharmacological action

A

Antagonize effect of leukotrienes to reduce airway edema and smooth muscle constriction

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110
Q

Montelukast: therapeutic use

A

Prevention and treatment of chronic asthma
Management of seasonal allergic rhinitis
Prevention of exercise induced bronchoconstriction

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111
Q

Montelukast: evaluation of effectiveness

A

Prevention/reduction of asthma symptoms
Decreased severity of allergic rhinitis
Prevention of exercise induced bronchoconstriction

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112
Q

What is the role of leukotriene modifiers in asthma management?

A

Long term management of persistent asthma not controlled by SABAs or corticosteroids

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113
Q

What is the mechanism of action for mast cell stabilizers?

A

Inhibiting release of histamine and other chemical mediators of inflammation from mast cells

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114
Q

Cromolyn: class

A

Mast cell stabilizer

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115
Q

Cromolyn: therapeutic use

A

Reducing airway inflammation to prevent asthma attacks

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116
Q

What must be remembered about administration of Cromolyn?

A

Has a short half life, so must be taken 4-6 times daily

May take several weeks to reach maximum therapeutic benefits

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117
Q

What is the mechanism of action for antihistamines?

A

Blocking action of histamine at H1 receptors

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118
Q

What are the most frequent uses for antihistamines?

A

Allergy symptoms
Motion sickness
Insomnia

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119
Q

What are the anticholinergic effects of antihistamines?

A

Increased HR
Urinary retention
Constipation
Blurred vision

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120
Q

Loratadine: class

A

Antihistamine

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121
Q

Loratadine: pharmacological action

A

Blocking peripheral effects of histamine released during allergic reactions

122
Q

Loratadine: therapeutic use

A

Relief of seasonal allergies
Management of chronic idiopathic urticaria
Management of hives

123
Q

Loratadine: evaluation of effectiveness

A

Decreased allergy symptoms

Management of hives and chronic idiopathic urticaria

124
Q

What is the benefit to a second generation antihistamine like loratadine?

A

Fewer anticholinergic side effects

125
Q

What is often the first line treatment of allergic rhinitis?

A

Intranasal corticosteroids

126
Q

Why are intranasal corticosteroids often the first line treatment for allergic rhinitis?

A

They produce virtually no serious adverse effects (in comparison to systemic corticosteroids)

127
Q

What is the mechanism of action for intranasal corticosteroids?

A

Decreased secretion of inflammatory mediators, reduced tissue edema, and mild vasoconstriction

128
Q

Why must intranasal corticosteroids be taken in advance of expected allergen exposure?

A

They take 1-3 weeks to reach peak effectiveness

129
Q

Sympathomimetics are also known as

A

Decongestants

130
Q

What do sympathomimetics activate?

A

Sympathetic nervous system

131
Q

What is the most serious side effect of intranasal sympathomimetics?

A

Rebound congestion (hypersecretion of mucous when drug wears off)

132
Q

How long should sympathomimetics be used?

A

No longer than 3-5 days at a time

133
Q

Why is the sale of pseudoephedrine carefully controlled?

A

It’s a starting chemical for meth synthesis

still sold OTC but closely controlled and tracked

134
Q

Why are sympathomimetics often combined with antihistamines?

A

To control other symptoms like sneezing and tearing eyes

135
Q

What are antitussives?

A

Cough suppressants

136
Q

What is the mechanism of action when opioids are used as a cough suppressant?

A

They raise the cough threshold in the CNS

137
Q

Why is there a low dependence potential when codeine is used as a cough suppressant?

A

Very low doses are used to suppress cough reflex

138
Q

What care must be taken when a patient who has asthma takes codeine as a cough suppressant?

A

Bronchoconstriction can occur

139
Q

Pseudoephedrine: class

A

Alpha adrenergic agonist

140
Q

Pseudoephedrine: pharmacological action

A

Stimulates alpha and beta adrenergic receptors to cause vasoconstriction in respiratory tract mucosa and possible bronchodilation

141
Q

Pseudoephedrine: therapeutic use

A

Management of nasal congestion associated with acute viral upper respiratory infection
Allergy management
Opening of Eustachian tubes in ear inflammation or infection

142
Q

Pseudoephedrine: evaluation of effectiveness

A

Decreased nasal/sinus/ear congestion

143
Q

What is the mechanism of action for dextromethorphan?

A

Raising cough threshold in CNS

144
Q

Does codeine or dextromethorphan have a higher potential for abuse?

A

Dextromethorphan

145
Q

What is the mechanism of action for expectorants?

A

Reduced viscosity of bronchial secretions so they can be removed more easily by coughing

146
Q

Guaifenesin: class

A

Expectorant

147
Q

Guaifenesin: Pharmacological action

A

Reduces viscosity of tenacious secretions by increasing respiratory tract secretions

148
Q

Guaifenesin: brand name

A

Robitussin

149
Q

Guaifenesin: therapeutic use

A

Cough associated with a viral upper respiratory infection

150
Q

Guaifenesin: evaluation of effectiveness

A

Easier mobilization/expectoration of mucus

151
Q

What is a benefit of guaifenesin?

A

Few adverse effects

152
Q

What is the most common use of guaifenesin?

A

Treatment of dry, non-productive cough

153
Q

What is the mechanism of action for mucolytics?

A

Break down the chemical structure of mucous molecules

154
Q

What is the primary use for mucolytics?

A

CF
Chronic bronchitis
Other diseases with lots of bronchial secretions

155
Q

Acetylcysteine: class

A

Mucolytic

156
Q

Acetylcysteine: pharmacological action

A

Degrades mucus, allowing for easier mobilization and expectoration

157
Q

Acetylcysteine: therapeutic use

A

Management of conditions thick mucous secretions

158
Q

Acetylcysteine: evaluation of effectiveness

A

Decreased dyspnea and clearing of lung sounds

159
Q

What is the route of administration for acetylcysteine?

A

Inhalation via nebulizer

160
Q

Loop diuretics: mechanism of action

A

Block Na and Cl reabsorption at the loop of Henle

161
Q

Loop diuretics: use

A

Excreting lots of water in a short period of time, such as in heart/liver/kidney failure.
Edema reduction

162
Q

Loop diuretics: adverse effects

A 
Dehydration 
Electrolyte imbalance 
Ototoxicity (furosemide)
Hypotension
Dizziness
163
Q

Loop diuretic: exemplar drug

A

Furosemide

164
Q

Thiazides diuretics: mechanism of action

A

Block sodium reabsorption in DCT to increase potassium and water excretion

165
Q

Thiazide diuretic: use

A

Mild-moderate HTN

Edema

166
Q

Thiazide diuretics: adverse effects

A

Dehydration

Electrolyte imbalance with over treatment

167
Q

Thiazide diuretics: exemplar drug

A

Hydrochlorothiazide

168
Q

Potassium sparing diuretics: mechanism

A

Antagonizes aldosterone to block sodium with minimal impact on potassium

169
Q

Potassium sparing diuretics: use

A

Edema/HTN when potassium needs to be preserved

170
Q

Potassium sparing diuretics: adverse effects

A

Headache
Fatigue
Mild hypokalemia

171
Q

Potassium sparing diuretics: exemplar drug

A

Spironolactone

172
Q

Osmotic diuretics: mechanism of action

A

Pulls water into the nephron at the PCT, loop of henle, and collecting duct, increasing water and electrolyte excretion

173
Q

Osmotic diuretics: use

A

Used rarely, and only in very specific circumstances

174
Q

Osmotic diuretics: adverse effects

A

Electrolyte imbalance, fatigue, N/V, hyponatremia, edema, convulsions, tachycardia

175
Q

Osmotic diuretics: exemplar drug

A

Mannitol

176
Q

Angiotensin-converting enzyme (ACE) inhibitor: mechanism

A

Block conversion of angiotensin I to angiotensin II, blocking vasoconstriction and aldosterone release and decreasing blood volume

177
Q

ACE inhibitor: use

A

Hypertension
Heart failure
MI

178
Q

ACE inhibitor: adverse effects

A

Dry, persistent cough
Postural hypotension
Hyperkalemia
Angioedema

179
Q

ACE inhibitor: exemplar

A

Lisinopril

180
Q

Calcium channel blockers: mechanism

A

Block calcium ion channels to relax cardiac and smooth muscle

181
Q

Calcium channel blockers: use

A

Hypertension
Angina pectoris
Dysrhythmias

182
Q

Calcium channel blockers: adverse effects

A 
Hepatotoxicity
MI
HF
Confusion
Headache
Fatigue
183
Q

Calcium channel blocker: exemplar

A

Diltiazem

184
Q

Aldosterone antagonist: mechanism

A

Blocks aldosterone receptors

185
Q

Aldosterone antagonists: use

A

HTN
HF
Edema
Post MI treatment

186
Q

Direct renin inhibitor: mechanism

A

Inhibit renin effects by binding to renin

187
Q

Direct renin inhibitor: use

A

Hypertension

188
Q

Direct renin inhibitor: adverse effects

A

Diarrhea
Cough
Flu like symptoms
Angioedema

189
Q

Direct renin inhibitor: exemplar

A

Aliskiren

190
Q

Adrenergic antagonist: mechanism of action

A

Blocks action at alpha one or alpha 2 adrenergic receptors to block SNS responses in the body

191
Q

Adrenergic antagonists: uses

A

HTN
Cardiovascular disorders
Angina pectoris

192
Q

Adrenergic antagonists: adverse effects

A 
Laryngospasm
Anaphylaxis 
Tachycardia
Dysrhythmias 
Sedation
Dizziness
193
Q

Adrenergic antagonist: exemplar

A

Clonadine

194
Q

Vasodilator: mechanism of action

A

Directly relaxes vascular smooth muscle

195
Q

Vasodilator: use

A

Hypertension

196
Q

Vasodilators: adverse effects

A 
Reflex tachycardia 
Severe hypotension
MI
Dysrhythmias 
Shock
Sodium and water retention
197
Q

Vasodilator: exemplar

A

Hydralazine

198
Q

What are medications such as nitroprusside used for? What are the parameters for use?

A

Hypertensive emergencies, with BP usually above 180/120

199
Q

What are some examples of hypertensive emergencies?

A

Poorly controlled primary hypertension
Head injury
Thyroid crisis
Eclampsia or pre-eclampsia

200
Q

Nitroprusside adverse effects

A

Hypotension

Blood flow restriction to brain and organs

201
Q

Beta-adrenergic blockers: mechanism of action

A

Block cardiac action of SNS and inhibit renin secretion, lowering heart rate and BP

202
Q

Beta adrenergic blockers: use

A

Heart failure

203
Q

Beta adrenergic blockers: exemplar

A

Metoprolol

204
Q

Cardiac glycosides: mechanism of action

A

Causes heart to beat more forcefully and slowly, increasing efficiency

205
Q

Cardiac glycoside: use

A

Heart failure symptom improvement

206
Q

Cardiac glycoside: exemplar

A

Digoxin

207
Q

Digoxin adverse effects/risks

A

Narrow therapeutic index

Can cause digitalization (tissue saturation)

208
Q

Phosphodiesterase inhibitors: mechanism of action

A

Blocking phosphodiesterase to increase calcium availability to heart muscle, increasing cardiac output

209
Q

Phosphodiesterase inhibitors: use

A

Acute heart failure

210
Q

Phosphodiesterase inhibitors: adverse effects

A

Serious toxicity
Ventricular dysrhythmias
Hypotension

211
Q

Under what conditions would adrenergic agonists be used in heart failure?

A

If heart is beating poorly/slowly and HR/BP need to be increased instead

212
Q

What are some adrenergic agonists that could be used to treat heart failure?

A

Epinephrine
Dopamine
Dobutamine

213
Q

What types of medications are used to treat angina?

A

Organic nitrites

Calcium channel blockers

214
Q

Organic nitrites: mechanism of action

A

Formation of nitric acid, which vasodilates vascular smooth muscle and decreases preload

215
Q

Organic nitrites: use

A

Angina

216
Q

Organic nitrites: adverse effects

A

Tolerance
Headaches
Orthostatic hypotension
Reflex tachycardia

217
Q

Organic nitrites: exemplars

A

Nitroglycerine

Isosorbide

218
Q

Statins: mechanism of action

A

Leads to less cholesterol biosynthesis, causing the liver to make more LDL receptors and excrete LDL from the body

219
Q

Statins: use

A

Control of hyperlipidemia

220
Q

Statins: exemplar

A

Atorvastatin

221
Q

Bile acid sequestrant: mechanism of action

A

Binding bile acids, which contain a lot of cholesterol. Also causes liver to make more LDL receptors, so it gets excreted from body

222
Q

Bile acid sequestrants: use

A

Lowering cholesterol

223
Q

Bile acid sequestrants: adverse effects

A

GI issues
Binding other drugs
Nutrient deficiencies

224
Q

Bile acid sequestrant: exemplar

A

Colesevelam

225
Q

Niacin: use (other than vitamin use)

A

Lowering lipid levels

226
Q

Niacin: mechanism of action

A

Decrease VLDL levels to lower serum triglycerides

227
Q

Fibric acid drug: mechanism of action

A

Activate lipoprotein lipase for the breakdown and elimination of triglyceride-rich particles

228
Q

Fibric acid drugs: use

A

Treatment of high triglycerides and VLDL levels

229
Q

Fibric acid drugs: adverse effects

A

GI symptoms

230
Q

Fibric acid drug: exemplar

A

Fenofibrate

231
Q

Cholesterol absorption inhibitor: action

A

Inhibit cholesterol absorption from food and inhibits reabsorption of cholesterol secreted in bile

232
Q

Examples of iron supplements

A 
Ferrous sulfate (oral)
Iron dextran (IM)
233
Q

Sulfadiazine: class

A

Sulfonamide (folic acid inhibitor antimicrobial)

234
Q

Sulfadiazine: use

A

UTI treatment (not first line treatment)

235
Q

Sulfadiazine: evaluation of effectiveness

A

Decreased UTI manifestations

236
Q

Sulfadiazine: teaching points

A

Can cause hypersensitivity and blood disorders
Wear sunscreen (photosensitivity)
Decreased contraceptive effectiveness
Do not take with potassium supplements

237
Q

Nitrofurantoin: class

A

Urinary tract antiseptic/antimicrobial

238
Q

Nitrofurantoin: action

A

Causes bacterial injury by damaging DNA

239
Q

Nitrofurantoin: use

A

Acute UTI treatment

Prophylaxis for recurrent lower UTIs

240
Q

Nitrofurantoin: evaluation of effectiveness

A

Decreased UTI manifestations

Negative urine cultures and lower WBC count

241
Q

Nitrofurantoin: client education/considerations

A

Can turn urine rust yellow or brown and stain teeth

Don’t use in pregnancy/childbirth

242
Q

Is sulfadiazine a first line treatment for UTIs?

A

No, due to prevalence of resistive strains

243
Q

Nitrofurantoin: teaching points

A

Take with food
Can turn urine rust yellow or brown and can stain teeth
Do not use during childbirth

244
Q

Ciprofloxacin: class

A

Floroquinolones (antibiotics)

245
Q

Ciprofloxacin: use

A

Urinary infections
Other infections
Anthrax prevention

246
Q

Ciprofloxacin: action

A

Inhibits an enzyme needed for DNA replication

247
Q

Ciprofloxacin: adverse effects

A

High incidence of N/V/D
Dysrhythmias
Can cause Achilles’ tendon rupture (dont give to kids under 18)

248
Q

Ciprofloxacin: evaluation of effectiveness

A

Decreased UTI manifestations/negative urine culture/lower WBC count

249
Q

Phenazopyridine: class

A

Urinary tract analgesic

250
Q

Phenazopyridine: action

A

Aso dye that acts as a local anesthetic on mucosa of urinary tract

251
Q

Phenazopyridine: use

A

Relieves manifestations of UTI (burning with urination, pain, urgency)

252
Q

Phenazopyridine: side effects

A

GI issues/pain
Headache
Dizziness

253
Q

Phenazopyridine: nursing considerations/teaching points

A

Give with food to decrease GI discomfort

Urine can change to red/orange and will stain

254
Q

Amoxicillin: class

A

Antibiotic

255
Q

What GI issue can amoxicillin be used to treat?

A

Peptic ulcer disease (by eradicating H. Pylori)

256
Q

Amoxicillin: side effects

A

Nausea
Vomiting
Diarrhea

257
Q

Nursing considerations when giving amoxicillin for PUD

A

Administer with food to minimize GI upset

258
Q

Ranitidine: class

A

Histamine receptor antagonist

259
Q

Ranitidine: mechanism of action

A

Blocks H2 receptors to suppress secretion of gastric acid and lower concentration of hydrogen ions in stomach

260
Q

Ranitidine: use

A

Prevention or treatment of gastric ulcers, GERD, hypersecretory conditions, heartburn, and acid indigestion

261
Q

Ranitidine: adverse

A

Constipation
Diarrhea
Nausea
High doses may cause impotence or loss of libido in men

262
Q

Ranitidine: interactions

A

Antacids can decrease absorption (dont give within one hour of each other)
May decrease iron and B12 absorption

263
Q

Omeprazole: class

A

Proton pump inhibitor

264
Q

Omeprazole: action

A

Blocks acid production in the stomach, reducing gastric acid secretion

265
Q

Omeprazole: use

A

Short term therapy of gastric/duodenal ulcers and GERD
Long term treatment of hypersecretory conditions
Stress ulcer prevention

266
Q

How long should omeprazole therapy be?

A

Between four and eight weeks (no longer than 8 if short term)

267
Q

Omeprazole: adverse

A 
Risk for low calcium levels/increased fracture risk
Hepatotoxicity 
Not approved for those under 18
NVD
Hypomagnesia
268
Q

Omeprazole: client education

A

Take before food
Monitor for s/s of GI bleeding
Take calcium and vitamin D supplements
Decrease alcohol, caffeine, and NSAID intake

269
Q

Sucralfate: class

A

Mucosal protectant

270
Q

Sucralfate: action

A

Acid of the stomach changes the drug into a protective barrier that adheres to ulcers in the GI tract

271
Q

Sucralfate: use

A

Treatment/maintenance of acute duodenal ulcers

Reduced acidity of gastric acid

272
Q

Sucralfate: administration

A

Take 4 times a day for effectiveness (3 meals and at bedtime)

273
Q

Sucralfate: adverse

A

Minimal adverse/systemic effects

Can cause constipation

274
Q

Aluminum hydroxide: class

A

Antacid

275
Q

Aluminum hydroxide: action

A

Neutralize/reduce activity of gastric acid

276
Q

Aluminum hydroxide: use

A

Treatment of peptic ulcers
Prevention of stress induced ulcers
Relief of GERD manifestations

277
Q

Aluminum hydroxide: adverse

A

Constipation
Fluid retention
Electrolyte imbalances

278
Q

Aluminum hydroxide: considerations for administration

A

Don’t give with other meds
Give other meds one hour before or after
Take with a small amount of water

279
Q

What happens to the minerals in antacids?

A

They are absorbed into circulation

280
Q

Misoprostol: class

A

Prostagladin E analog

281
Q

Misoprostol: use

A

Treatment of ulcers caused by high doses of NSAIDs

Relief of diarrhea and abdominal cramping

282
Q

Misoprostol: action

A

Acts as endogenous prostaglandin in GI tract to decrease acid secretion and stimulate the secretion of protective mucous

283
Q

Misoprostol: adverse

A

Pregnancy category X

284
Q

Loperamide: class

A

Antidiarrheal

285
Q

Loperamide: action

A

Activates opioid receptors in the GI tract to decrease intestinal motility and increase water and sodium absorption into intestine

286
Q

Loperamide: use

A

Diarrhea relief

287
Q

Loperamide: adverse

A

High doses can have opiate effects (drowsiness, lightheadedness, nausea, dizziness)

288
Q

Loperamide: administration/patient education

A

Drink small amounts of electrolytes for first 24 hours
Avoid caffeine
Do not use with food poisoning

289
Q

Metoclopramide: class

A

Phenothiazide/anti-emetic

290
Q

Metoclopramide: action

A

Blocking dopamine and serotonin receptors in GI tract to reduce stimulus to empty bowels

291
Q

Metoclopramide: use

A

Controlling post-operative and chemo-induced N/V

GERD management

292
Q

Metoclopramide: adverse

A

CNS depression/sedation
Anticholinergic effects
Extrapyramidal symptoms

293
Q

Alosetron: class

A

Meds for IBS with diarrhea

294
Q

Alosetron: action

A

Selective block of 5-HT3 receptors to slow stool

295
Q

Alosetron: use

A

IBS-D

296
Q

Alosetron: adverse

A

Serious GI issues (Constipation, nausea, abdominal discomfort, GI bleeding)
Rash
Ischemic colitis
use is limited due to serious side effects

297
Q

Sulfasalazine: class

A

5-aminosalicylates

298
Q

Sulfasalazine: use

A

Treatment of IBS with constipation

299
Q

Sulfasalazine: action

A

Decreased inflammation by inhibiting prostaglandin synthesis

300
Q

Sulfasalazine: adverse

A 
N/V
Anorexia
Abdominal pain
Headaches 
Impaired male fertility
Blood disorders
301
Q

Sulfasalazine: things to monitor

A

Warfarin levels (may increase)
Digoxin levels (may decrease)
Iron/folic acid absorption
CBC

Krystan: Semester Two Nursing School (13 decks)

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