2820 Pharmacology Exam 2 Flashcards

(301 cards)

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
Naproxen: evaluation of effectiveness
Reduced pain Increased joint mobility Fever reduction
26
Acetaminophen: class
Non-opioid analgesic
27
Acetaminophen: pharmacological action
Inhibits prostaglandin synthesis (without anti-inflammatory effects)
28
Acetaminophen: therapeutic use
Pain | Fever
29
Acetaminophen: evaluation of effectiveness
Pain and fever relief
30
What are some examples of opioid agonists?
``` Morphine Fentanyl Merperidine Codeine Oxycodone Hydromorphone ```
31
What is the gold standard medication for pain management?
Morphine
32
How do opioid agonists work in the body?
They bind to and activate mu and kappa receptors
33
Morphine: class
Opioid agonist
34
Morphine: pharmacological action
Bind to opiate receptors in CNS, altering pain perception and response while depressing CNS
35
Morphine: therapeutic use
Severe pain when other treatment options are inadequate Pulmonary edema MI pain
36
Morphine: evaluation of effectiveness
Decreased pain without altered LOC or respiratory status | Decreased symptoms of pulmonary edema
37
Fentanyl: class
Opioid agonist
38
Fentanyl: pharmacological action
Binds to opiate receptors in CNS, altering pain perception/response
39
Fentanyl: therapeutic use
Supplement to anesthesia | Induction and maintenance of anesthesia
40
Fentanyl: evaluation of effectiveness
Quiescence Reduced motor activity Analgesia
41
Oxycodone: class
Opioid agonist
42
Oxycodone: pharmacological action
Binding to opiate receptors in CNS
43
Oxycodone: therapeutic use
Moderate to severe pain requiring round the clock treatment
44
Oxycodone: evaluation of effectiveness
Decreased pain severity without altered level of consciousness or respiratory status
45
Naloxone: class
Opioid antagonist
46
Naloxone: pharmacological action
Competitively blocks opioid receptors to block effects of opioids
47
Naloxone: therapeutic use
Reversal of CNS depression because of opioid overdose
48
Naloxone: evaluation of effectiveness
Adequate ventilation following opioid excess | Alertness without pain or withdrawal symptoms
49
What should the nurse remember about administering naloxone?
It has a very short half life, so will need to be administered frequently for effectiveness (and administered until opioids are out of system)
50
Amitriptyline: class
Tricyclic Antidepressant
51
Amitriptyline: pharmacological action
Increases synaptic concentration of serotonin and norepinephrine (potentiates their effects)
52
Amitriptyline: therapeutic use
Depression Anxiety Also found to help with chronic pain syndromes and insomnia
53
Amitriptyline: evaluation of effectiveness
Increased sense of well-being Renewed interest in surroundings Improved appetite, energy level, and sleep Decreased chronic pain
54
Gabapentin: class
Anticonvulsant/analgesic adjunct/mood stabilizer
55
Gabapentin: pharmacological action
Uncertain, but may inhibit excitatory neuron activity and affect amino acid transport
56
Gabapentin: therapeutic uses
``` Partial seizures Neuralgia Restless leg syndrome Neuropathic pain Diabetic neuropathy Depression Anxiety ```
57
Gabapentin: evaluation of effectiveness
``` Decreased seizure frequency Decreased pain Decreased migraines Increased mood stability Decreased effects of restless leg syndrome ```
58
Sumatriptan: class
5HT1 agonist (vascular headache suppressant)
59
Sumatriptan: pharmacological action
Selective agonist of 5HT1 vascular serotonin receptor sites, causing vasoconstriction in large intracranial arteries
60
Sumatriptan: therapeutic use
Relief of acute migraine attack
61
Sumatriptan: evaluation of effectiveness
Migraine relief
62
What is the mechanism of action for beta 2 adrenergic agonists?
Activate SNS to relax bronchial smooth muscle, causing bronchodilation
63
What is a drawback to beta agonists?
No anti-inflammatory ability so they cannot help with asthma inflammation
64
What diseases are beta agonists used for primarily?
Asthma, COPD, and cystic fibrosis
65
What is the benefit of short acting beta agonists?
Rapid onset of action
66
What are short acting beta agonists (SABAs) prescribed for?
Preventing or terminating an asthma attack
67
SABAs are also known as
Rescue drugs or a rescue inhaler
68
How long do the effects of SABAs last?
2-6 hours
69
Albuterol: class
Beta 2 adrenergic agonist
70
Albuterol: pharmacological action
Bind to beta 2 adrenergic receptors in airway to decrease intracellular calcium and relax smooth muscle in the airway
71
Albuterol: therapeutic use
Treatment or prevention of bronchospasm in COPD or asthma
72
Albuterol: evaluation of effectiveness
Prevention or relief of bronchospasm
73
How long do the effects of long acting beta agonists (LABAs) last?
Up to 12 hours
74
Why do LABAs have a black box warning?
Increased risk of asthma related deaths, because effects are not immediate and patient is in trouble if they take them during an acute attack
75
What is the benefit of LABA’s?
Minimal systemic effects or toxicity
76
Salmeterol: class
Beta 2 adrenergic agonist
77
Salmeterol: pharmacological action
Causes accumulation of cAMP at beta 2 adrenergic receptors in the lungs to cause bronchodilation
78
Salmeterol: therapeutic use
Prevention of bronchospasm in patients with poorly controlled asthma Prevention of exercise induced asthma
79
Salmeterol: evaluation of effectiveness
Prevention of exercise induced asthma | Prevention of bronchospam or reduced number of acute asthma attacks
80
What is the most common route of administration of beta agonists for respiratory conditions?
Inhalation
81
Why do inhaled beta agonists cause minimal systemic toxicity?
Only small amounts are absorbed into the body
82
What may happen with chronic use of beta agonists?
Tolerance can develop, leading to shorter duration of action
83
What does increased use of beta agonists over a period of hours or days indicate?
Rapidly deteriorating/poorly managed condition that needs medical intervention
84
What is the mechanism of action for anticholinergics?
Compete with ACh for binding at muscarinic receptors, blocking parasympathetic response (bronchodilation occurs)
85
Ipratropium: class
Anticholinergic
86
Ipratropium: pharmacological action
Inhibits cholinergic receptors in bronchial smooth muscle, leading to local bronchodilation
87
Ipratropium: therapeutic use
Maintenance therapy of reversible airway obstruction due to COPD
88
Ipratropium: evaluation of effectiveness
Decreased dyspnea Improved breath sounds Decreased rhinorrhea
89
Why is ipratropium the most frequently prescribed anticholinergic for COPD?
Slower onset of action with less intense bronchodilation than beta agonists
90
What is the first line treatment combination for COPD?
Ipratropium and albuterol
91
What is the benefit of combining ipratropium with a beta agonist?
Greater and more prolonged bronchodilation than either med can provide separately
92
What is the primary use for methylxanthines?
Long term management of persistent asthma that is unresponsive to beta agonists or corticosteroids
93
How do methylxanthines work?
They are chemically similar to caffeine, and relax muscles in airways
94
Why are methylxanthines infrequently prescribed?
Narrow safety margin, especially with prolonged use
95
What are two examples of methylxanthines?
Theophylline and aminophylline
96
What is the mechanism of action for corticosteroids?
Dampen activity of inflammatory cells and increase production of anti-inflammatory mediators
97
What is the effect of corticosteroids on bronchial smooth muscle?
They sensitize bronchial smooth muscle to respond to beta agonist stimulation (often used in conjunction)
98
What is the intended use of inhaled corticosteroids?
Preventing asthma attacks
99
When might a systemic corticosteroid be used to treat asthma?
Severe, unstable asthma that is unresponsive to other treatment. Intended for short term use only
100
What are the adverse effects of using using systemic corticosteroids for more than 10 days?
Adrenal gland suppression/atrophy Peptic ulcers Hyperglycemia Growth retardation in children
101
Why can you not stop taking systemic corticosteroids abruptly?
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
102
What can long term systemic corticosteroid use cause?
Cushing’s syndrome
103
Prednisone: class
Corticosteroid (systemic)
104
Prednisone: pharmacological action
Suppress inflammation and normal immune response
105
Prednisone: therapeutic use
Asthma | Other things unrelated to oxygenation
106
Prednisone: evaluation of effectiveness
Decrease in symptoms with minimal systemic effects
107
What are leukotrienes?
Bodily mediators of immune response involved in allergic and asthmatic reactions. They promote airway edema and inflammation
108
Montelukast: class
Leukotriene antagonist
109
Monteleukast: pharmacological action
Antagonize effect of leukotrienes to reduce airway edema and smooth muscle constriction
110
Montelukast: therapeutic use
Prevention and treatment of chronic asthma Management of seasonal allergic rhinitis Prevention of exercise induced bronchoconstriction
111
Montelukast: evaluation of effectiveness
Prevention/reduction of asthma symptoms Decreased severity of allergic rhinitis Prevention of exercise induced bronchoconstriction
112
What is the role of leukotriene modifiers in asthma management?
Long term management of persistent asthma not controlled by SABAs or corticosteroids
113
What is the mechanism of action for mast cell stabilizers?
Inhibiting release of histamine and other chemical mediators of inflammation from mast cells
114
Cromolyn: class
Mast cell stabilizer
115
Cromolyn: therapeutic use
Reducing airway inflammation to prevent asthma attacks
116
What must be remembered about administration of Cromolyn?
Has a short half life, so must be taken 4-6 times daily | May take several weeks to reach maximum therapeutic benefits
117
What is the mechanism of action for antihistamines?
Blocking action of histamine at H1 receptors
118
What are the most frequent uses for antihistamines?
Allergy symptoms Motion sickness Insomnia
119
What are the anticholinergic effects of antihistamines?
Increased HR Urinary retention Constipation Blurred vision
120
Loratadine: class
Antihistamine
121
Loratadine: pharmacological action
Blocking peripheral effects of histamine released during allergic reactions
122
Loratadine: therapeutic use
Relief of seasonal allergies Management of chronic idiopathic urticaria Management of hives
123
Loratadine: evaluation of effectiveness
Decreased allergy symptoms | Management of hives and chronic idiopathic urticaria
124
What is the benefit to a second generation antihistamine like loratadine?
Fewer anticholinergic side effects
125
What is often the first line treatment of allergic rhinitis?
Intranasal corticosteroids
126
Why are intranasal corticosteroids often the first line treatment for allergic rhinitis?
They produce virtually no serious adverse effects (in comparison to systemic corticosteroids)
127
What is the mechanism of action for intranasal corticosteroids?
Decreased secretion of inflammatory mediators, reduced tissue edema, and mild vasoconstriction
128
Why must intranasal corticosteroids be taken in advance of expected allergen exposure?
They take 1-3 weeks to reach peak effectiveness
129
Sympathomimetics are also known as
Decongestants
130
What do sympathomimetics activate?
Sympathetic nervous system
131
What is the most serious side effect of intranasal sympathomimetics?
Rebound congestion (hypersecretion of mucous when drug wears off)
132
How long should sympathomimetics be used?
No longer than 3-5 days at a time
133
Why is the sale of pseudoephedrine carefully controlled?
It’s a starting chemical for meth synthesis | *still sold OTC but closely controlled and tracked*
134
Why are sympathomimetics often combined with antihistamines?
To control other symptoms like sneezing and tearing eyes
135
What are antitussives?
Cough suppressants
136
What is the mechanism of action when opioids are used as a cough suppressant?
They raise the cough threshold in the CNS
137
Why is there a low dependence potential when codeine is used as a cough suppressant?
Very low doses are used to suppress cough reflex
138
What care must be taken when a patient who has asthma takes codeine as a cough suppressant?
Bronchoconstriction can occur
139
Pseudoephedrine: class
Alpha adrenergic agonist
140
Pseudoephedrine: pharmacological action
Stimulates alpha and beta adrenergic receptors to cause vasoconstriction in respiratory tract mucosa and possible bronchodilation
141
Pseudoephedrine: therapeutic use
Management of nasal congestion associated with acute viral upper respiratory infection Allergy management Opening of Eustachian tubes in ear inflammation or infection
142
Pseudoephedrine: evaluation of effectiveness
Decreased nasal/sinus/ear congestion
143
What is the mechanism of action for dextromethorphan?
Raising cough threshold in CNS
144
Does codeine or dextromethorphan have a higher potential for abuse?
Dextromethorphan
145
What is the mechanism of action for expectorants?
Reduced viscosity of bronchial secretions so they can be removed more easily by coughing
146
Guaifenesin: class
Expectorant
147
Guaifenesin: Pharmacological action
Reduces viscosity of tenacious secretions by increasing respiratory tract secretions
148
Guaifenesin: brand name
Robitussin
149
Guaifenesin: therapeutic use
Cough associated with a viral upper respiratory infection
150
Guaifenesin: evaluation of effectiveness
Easier mobilization/expectoration of mucus
151
What is a benefit of guaifenesin?
Few adverse effects
152
What is the most common use of guaifenesin?
Treatment of dry, non-productive cough
153
What is the mechanism of action for mucolytics?
Break down the chemical structure of mucous molecules
154
What is the primary use for mucolytics?
CF Chronic bronchitis Other diseases with lots of bronchial secretions
155
Acetylcysteine: class
Mucolytic
156
Acetylcysteine: pharmacological action
Degrades mucus, allowing for easier mobilization and expectoration
157
Acetylcysteine: therapeutic use
Management of conditions thick mucous secretions
158
Acetylcysteine: evaluation of effectiveness
Decreased dyspnea and clearing of lung sounds
159
What is the route of administration for acetylcysteine?
Inhalation via nebulizer
160
Loop diuretics: mechanism of action
Block Na and Cl reabsorption at the loop of Henle
161
Loop diuretics: use
Excreting lots of water in a short period of time, such as in heart/liver/kidney failure. Edema reduction
162
Loop diuretics: adverse effects
``` Dehydration Electrolyte imbalance Ototoxicity (furosemide) Hypotension Dizziness ```
163
Loop diuretic: exemplar drug
Furosemide
164
Thiazides diuretics: mechanism of action
Block sodium reabsorption in DCT to increase potassium and water excretion
165
Thiazide diuretic: use
Mild-moderate HTN | Edema
166
Thiazide diuretics: adverse effects
Dehydration | Electrolyte imbalance with over treatment
167
Thiazide diuretics: exemplar drug
Hydrochlorothiazide
168
Potassium sparing diuretics: mechanism
Antagonizes aldosterone to block sodium with minimal impact on potassium
169
Potassium sparing diuretics: use
Edema/HTN when potassium needs to be preserved
170
Potassium sparing diuretics: adverse effects
Headache Fatigue Mild hypokalemia
171
Potassium sparing diuretics: exemplar drug
Spironolactone
172
Osmotic diuretics: mechanism of action
Pulls water into the nephron at the PCT, loop of henle, and collecting duct, increasing water and electrolyte excretion
173
Osmotic diuretics: use
Used rarely, and only in very specific circumstances
174
Osmotic diuretics: adverse effects
Electrolyte imbalance, fatigue, N/V, hyponatremia, edema, convulsions, tachycardia
175
Osmotic diuretics: exemplar drug
Mannitol
176
Angiotensin-converting enzyme (ACE) inhibitor: mechanism
Block conversion of angiotensin I to angiotensin II, blocking vasoconstriction and aldosterone release and decreasing blood volume
177
ACE inhibitor: use
Hypertension Heart failure MI
178
ACE inhibitor: adverse effects
Dry, persistent cough Postural hypotension Hyperkalemia Angioedema
179
ACE inhibitor: exemplar
Lisinopril
180
Calcium channel blockers: mechanism
Block calcium ion channels to relax cardiac and smooth muscle
181
Calcium channel blockers: use
Hypertension Angina pectoris Dysrhythmias
182
Calcium channel blockers: adverse effects
``` Hepatotoxicity MI HF Confusion Headache Fatigue ```
183
Calcium channel blocker: exemplar
Diltiazem
184
Aldosterone antagonist: mechanism
Blocks aldosterone receptors
185
Aldosterone antagonists: use
HTN HF Edema Post MI treatment
186
Direct renin inhibitor: mechanism
Inhibit renin effects by binding to renin
187
Direct renin inhibitor: use
Hypertension
188
Direct renin inhibitor: adverse effects
Diarrhea Cough Flu like symptoms Angioedema
189
Direct renin inhibitor: exemplar
Aliskiren
190
Adrenergic antagonist: mechanism of action
Blocks action at alpha one or alpha 2 adrenergic receptors to block SNS responses in the body
191
Adrenergic antagonists: uses
HTN Cardiovascular disorders Angina pectoris
192
Adrenergic antagonists: adverse effects
``` Laryngospasm Anaphylaxis Tachycardia Dysrhythmias Sedation Dizziness ```
193
Adrenergic antagonist: exemplar
Clonadine
194
Vasodilator: mechanism of action
Directly relaxes vascular smooth muscle
195
Vasodilator: use
Hypertension
196
Vasodilators: adverse effects
``` Reflex tachycardia Severe hypotension MI Dysrhythmias Shock Sodium and water retention ```
197
Vasodilator: exemplar
Hydralazine
198
What are medications such as nitroprusside used for? What are the parameters for use?
Hypertensive emergencies, with BP usually above 180/120
199
What are some examples of hypertensive emergencies?
Poorly controlled primary hypertension Head injury Thyroid crisis Eclampsia or pre-eclampsia
200
Nitroprusside adverse effects
Hypotension | Blood flow restriction to brain and organs
201
Beta-adrenergic blockers: mechanism of action
Block cardiac action of SNS and inhibit renin secretion, lowering heart rate and BP
202
Beta adrenergic blockers: use
Heart failure
203
Beta adrenergic blockers: exemplar
Metoprolol
204
Cardiac glycosides: mechanism of action
Causes heart to beat more forcefully and slowly, increasing efficiency
205
Cardiac glycoside: use
Heart failure symptom improvement
206
Cardiac glycoside: exemplar
Digoxin
207
Digoxin adverse effects/risks
Narrow therapeutic index | Can cause digitalization (tissue saturation)
208
Phosphodiesterase inhibitors: mechanism of action
Blocking phosphodiesterase to increase calcium availability to heart muscle, increasing cardiac output
209
Phosphodiesterase inhibitors: use
Acute heart failure
210
Phosphodiesterase inhibitors: adverse effects
Serious toxicity Ventricular dysrhythmias Hypotension
211
Under what conditions would adrenergic agonists be used in heart failure?
If heart is beating poorly/slowly and HR/BP need to be increased instead
212
What are some adrenergic agonists that could be used to treat heart failure?
Epinephrine Dopamine Dobutamine
213
What types of medications are used to treat angina?
Organic nitrites | Calcium channel blockers
214
Organic nitrites: mechanism of action
Formation of nitric acid, which vasodilates vascular smooth muscle and decreases preload
215
Organic nitrites: use
Angina
216
Organic nitrites: adverse effects
Tolerance Headaches Orthostatic hypotension Reflex tachycardia
217
Organic nitrites: exemplars
Nitroglycerine | Isosorbide
218
Statins: mechanism of action
Leads to less cholesterol biosynthesis, causing the liver to make more LDL receptors and excrete LDL from the body
219
Statins: use
Control of hyperlipidemia
220
Statins: exemplar
Atorvastatin
221
Bile acid sequestrant: mechanism of action
Binding bile acids, which contain a lot of cholesterol. Also causes liver to make more LDL receptors, so it gets excreted from body
222
Bile acid sequestrants: use
Lowering cholesterol
223
Bile acid sequestrants: adverse effects
GI issues Binding other drugs Nutrient deficiencies
224
Bile acid sequestrant: exemplar
Colesevelam
225
Niacin: use (other than vitamin use)
Lowering lipid levels
226
Niacin: mechanism of action
Decrease VLDL levels to lower serum triglycerides
227
Fibric acid drug: mechanism of action
Activate lipoprotein lipase for the breakdown and elimination of triglyceride-rich particles
228
Fibric acid drugs: use
Treatment of high triglycerides and VLDL levels
229
Fibric acid drugs: adverse effects
GI symptoms
230
Fibric acid drug: exemplar
Fenofibrate
231
Cholesterol absorption inhibitor: action
Inhibit cholesterol absorption from food and inhibits reabsorption of cholesterol secreted in bile
232
Examples of iron supplements
``` Ferrous sulfate (oral) Iron dextran (IM) ```
233
Sulfadiazine: class
Sulfonamide (folic acid inhibitor antimicrobial)
234
Sulfadiazine: use
UTI treatment (not first line treatment)
235
Sulfadiazine: evaluation of effectiveness
Decreased UTI manifestations
236
Sulfadiazine: teaching points
Can cause hypersensitivity and blood disorders Wear sunscreen (photosensitivity) Decreased contraceptive effectiveness Do not take with potassium supplements
237
Nitrofurantoin: class
Urinary tract antiseptic/antimicrobial
238
Nitrofurantoin: action
Causes bacterial injury by damaging DNA
239
Nitrofurantoin: use
Acute UTI treatment | Prophylaxis for recurrent lower UTIs
240
Nitrofurantoin: evaluation of effectiveness
Decreased UTI manifestations | Negative urine cultures and lower WBC count
241
Nitrofurantoin: client education/considerations
Can turn urine rust yellow or brown and stain teeth | Don’t use in pregnancy/childbirth
242
Is sulfadiazine a first line treatment for UTIs?
No, due to prevalence of resistive strains
243
Nitrofurantoin: teaching points
Take with food Can turn urine rust yellow or brown and can stain teeth Do not use during childbirth
244
Ciprofloxacin: class
Floroquinolones (antibiotics)
245
Ciprofloxacin: use
Urinary infections Other infections Anthrax prevention
246
Ciprofloxacin: action
Inhibits an enzyme needed for DNA replication
247
Ciprofloxacin: adverse effects
High incidence of N/V/D Dysrhythmias Can cause Achilles’ tendon rupture (dont give to kids under 18)
248
Ciprofloxacin: evaluation of effectiveness
Decreased UTI manifestations/negative urine culture/lower WBC count
249
Phenazopyridine: class
Urinary tract analgesic
250
Phenazopyridine: action
Aso dye that acts as a local anesthetic on mucosa of urinary tract
251
Phenazopyridine: use
Relieves manifestations of UTI (burning with urination, pain, urgency)
252
Phenazopyridine: side effects
GI issues/pain Headache Dizziness
253
Phenazopyridine: nursing considerations/teaching points
Give with food to decrease GI discomfort | Urine can change to red/orange and will stain
254
Amoxicillin: class
Antibiotic
255
What GI issue can amoxicillin be used to treat?
Peptic ulcer disease (by eradicating H. Pylori)
256
Amoxicillin: side effects
Nausea Vomiting Diarrhea
257
Nursing considerations when giving amoxicillin for PUD
Administer with food to minimize GI upset
258
Ranitidine: class
Histamine receptor antagonist
259
Ranitidine: mechanism of action
Blocks H2 receptors to suppress secretion of gastric acid and lower concentration of hydrogen ions in stomach
260
Ranitidine: use
Prevention or treatment of gastric ulcers, GERD, hypersecretory conditions, heartburn, and acid indigestion
261
Ranitidine: adverse
Constipation Diarrhea Nausea High doses may cause impotence or loss of libido in men
262
Ranitidine: interactions
Antacids can decrease absorption (dont give within one hour of each other) May decrease iron and B12 absorption
263
Omeprazole: class
Proton pump inhibitor
264
Omeprazole: action
Blocks acid production in the stomach, reducing gastric acid secretion
265
Omeprazole: use
Short term therapy of gastric/duodenal ulcers and GERD Long term treatment of hypersecretory conditions Stress ulcer prevention
266
How long should omeprazole therapy be?
Between four and eight weeks (no longer than 8 if short term)
267
Omeprazole: adverse
``` Risk for low calcium levels/increased fracture risk Hepatotoxicity Not approved for those under 18 NVD Hypomagnesia ```
268
Omeprazole: client education
Take before food Monitor for s/s of GI bleeding Take calcium and vitamin D supplements Decrease alcohol, caffeine, and NSAID intake
269
Sucralfate: class
Mucosal protectant
270
Sucralfate: action
Acid of the stomach changes the drug into a protective barrier that adheres to ulcers in the GI tract
271
Sucralfate: use
Treatment/maintenance of acute duodenal ulcers | Reduced acidity of gastric acid
272
Sucralfate: administration
Take 4 times a day for effectiveness (3 meals and at bedtime)
273
Sucralfate: adverse
Minimal adverse/systemic effects | Can cause constipation
274
Aluminum hydroxide: class
Antacid
275
Aluminum hydroxide: action
Neutralize/reduce activity of gastric acid
276
Aluminum hydroxide: use
Treatment of peptic ulcers Prevention of stress induced ulcers Relief of GERD manifestations
277
Aluminum hydroxide: adverse
Constipation Fluid retention Electrolyte imbalances
278
Aluminum hydroxide: considerations for administration
Don’t give with other meds Give other meds one hour before or after Take with a small amount of water
279
What happens to the minerals in antacids?
They are absorbed into circulation
280
Misoprostol: class
Prostagladin E analog
281
Misoprostol: use
Treatment of ulcers caused by high doses of NSAIDs | Relief of diarrhea and abdominal cramping
282
Misoprostol: action
Acts as endogenous prostaglandin in GI tract to decrease acid secretion and stimulate the secretion of protective mucous
283
Misoprostol: adverse
Pregnancy category X
284
Loperamide: class
Antidiarrheal
285
Loperamide: action
Activates opioid receptors in the GI tract to decrease intestinal motility and increase water and sodium absorption into intestine
286
Loperamide: use
Diarrhea relief
287
Loperamide: adverse
High doses can have opiate effects (drowsiness, lightheadedness, nausea, dizziness)
288
Loperamide: administration/patient education
Drink small amounts of electrolytes for first 24 hours Avoid caffeine Do not use with food poisoning
289
Metoclopramide: class
Phenothiazide/anti-emetic
290
Metoclopramide: action
Blocking dopamine and serotonin receptors in GI tract to reduce stimulus to empty bowels
291
Metoclopramide: use
Controlling post-operative and chemo-induced N/V | GERD management
292
Metoclopramide: adverse
CNS depression/sedation Anticholinergic effects Extrapyramidal symptoms
293
Alosetron: class
Meds for IBS with diarrhea
294
Alosetron: action
Selective block of 5-HT3 receptors to slow stool
295
Alosetron: use
IBS-D
296
Alosetron: adverse
Serious GI issues (Constipation, nausea, abdominal discomfort, GI bleeding) Rash Ischemic colitis **use is limited due to serious side effects**
297
Sulfasalazine: class
5-aminosalicylates
298
Sulfasalazine: use
Treatment of IBS with constipation
299
Sulfasalazine: action
Decreased inflammation by inhibiting prostaglandin synthesis
300
Sulfasalazine: adverse
``` N/V Anorexia Abdominal pain Headaches Impaired male fertility Blood disorders ```
301
Sulfasalazine: things to monitor
Warfarin levels (may increase) Digoxin levels (may decrease) Iron/folic acid absorption CBC