Module 05: Respiratory Pharmacology Flashcards
1
Q
This is an infection that involves the upper part of the respiratory system. This includes the nose, the throat, and the bronchi.
A
Upper Respiratory Tract Infection or Common Cold
2
Q
What are signs and symptoms of Upper Respiratory Tract Infection or Common Cold?
A
(A) Nasal congestion
(B) Sneezing
(C) Fatigue
(D) Body Aches
3
Q
What are the different types of supportive measures for Upper Respiratory Tract Infection or Common Cold?
A
(A) Rest adequately and increase oral fluid intake
(B) Sore throat (consume throat lozenges)
(C) Nasal congestion or stuffiness (take over the counter nasal decongestant)
(D) Cough and fevers (take an over the counter cough or fever reducer medicine)
4
Q
What are the categories of upper respiratory medications?
A
(A) Antihistamines (first generation and second generation)
(B) Nasal Decongestants
(C) Intranasal Glucocorticoids
(D) Antitussives
(E) Expectorants
(F) Mucolytics
5
Q
This upper respiratory medication is utilized to treat acute and allergic rhinitis.
A
Antihistamines
6
Q
What is the mechanism of action of antihistamines?
A
(A) Competes with histamine for receptor sites preventing histamine response.
(B) Reduces nasopharyngeal secretions, itching and sneezing
7
Q
What are the contraindications or cautions of using antihistamine?
A
(A) Severe liver disease
(B) Narrow angle glaucoma
(C) Urinary retention
8
Q
When did first generation antihistamines become available for general use?
A
1942 (Still used today)
9
Q
These medications work by affecting the histamine receptors in the brain and spinal cord.
A
First-generation antihistamines
10
Q
What are some examples of first-generation antihistamines?
A
(A) Brompheniramine (Children’s Dimetapp Cold)
(B) Diphenhydramine (Benadryl)
11
Q
What are some defining characteristics of first-generation antihistamines?
A
They go through the blood-brain barrier and cause sleepiness.
12
Q
When do first-generation antihistamines start to take an effect?
A
In about 30 to 60 minutes and last four to six hours.
13
Q
This is known as the most popular first-generation antihistamine, especially for emergency use. This can be found in some over-the-counter antihistamines.
A
Chlorpheniramine
14
Q
What are the side effects of first-generation antihistamines (besides drowsiness)?
A
(A) Dry mouth and eyes
(B) Blurry vision
(C) Headaches and dizziness
(D) Lowered blood pressure
(E) Mucous thickening
(F) Increased heart rate
(G) Constipation
(H) Trouble urinating
15
Q
These medications are able to reduce the inflammation caused by allergies and are favored both because they have fewer side effects and can be more effective in treating allergy symptoms.
A
Second-generation antihistamines
16
Q
What are some defining characteristics of second-generation antihistamines?
A
(A) Can be taken orally, nasally, IM or IV or via an eye dropper.
(B) Typically last for up to 24 hours.
17
Q
What are some side effects of second-generation antihistamines?
A
(A) Headache
(B) Cough
(C) Fatigue
(D) Sore throat
(E) Stomach pain
(F) Nausea or vomiting
18
Q
These medications may stimulate alpha adrenergic receptors.
A
Nasal Decongestants
19
Q
Nasal decongestants stimulate alpha adrenergic receptors by:
A
(A) Producing nasal vasoconstriction
(B) Shrinking nasal mucous membranes
(C) Reducing nasal secretion
20
Q
How are nasal decongestants administrated?
A
(A) Nasal Spray
(B) Nasal drops
(C) Tablet and capsule
(D) Liquid
21
Q
What are some drug to drug interactions that one should take note of when taking nasal decongestants?
A
May increase restlessness and palpitations when consumed with caffeine (i.e. coffee or tea)
22
Q
What are some examples of nasal decongestants?
A
(A) Oxymetazoline (Afrin)
(B) Naphazoline (Allerest)
(C) Pseudoephedrine (Sudafed)
23
Q
What are some side effects of nasal decongestants?
A
(A) Nervousness
(B) Jitters
(C) Restless
(D) Alpha-adrenergic effect (hypertension and hyperglycemia)
24
Q
What are some nursing implications that one should take note of when administering nasal decongestants to a patient?
A
(A) It causes rebound congestion if used for over 5 days.
(B) Increase fluid intake
25
What is the mechanism of action of intranasal glucocorticoids?
Anti-inflammatory
26
This medication is used to to treat allergic rhinitis and may be used alone or in combination with H1 antihistamines.
Intranasal Glucocorticoids
27
What are some contraindications and cautions of intranasal glucocorticoids?
Presence of acute infection (mucous)
28
Intranasal glucocorticoids are characterized to be like:
Cortisone-like medications
29
How can intranasal glucocorticoids be administered to the patient?
It can be sprayed or inhaled into the nose to help relieve stuffy nose, irritation, and discomfort of hay fever and other allergies and nasal problems.
30
Intranasal glucocorticoids are also used to prevent what?
To prevent nasal polyps from growing back after they have been removed by surgery.
31
Are Intranasal glucocorticoids prescription drugs or over the counter medications?
PRESCRIPTION ONLY MEDICATIONS
32
What are the dosage forms of intranasal glucocorticoids?
(A) Aerosol liquid
(B) Implant
(C) Spray
33
What are some side effects of intranasal glucocorticoids?
(A) Local burning
(B) Irritation
(C) Dryness of mucosa
(D) Headache
34
What are some nursing implications that one should take note of when administering intranasal glucocorticoids to a patient?
(A) Teach proper administration.
(B) Clear nasal passages before administration.
(C) Assess for the development of acute infection.
35
What is the mechanism of action of antitussives?
Thought to work by inhibiting a coordinating region for coughing located in the brain stem, disrupting the reflex arc; the exact mechanism is unknown.
36
These medications are used for temporary relief of coughs without phlegm that are caused by certain infections of the air passages (such as sinusitis and common cold).
Antitussives
37
When should antitussives be considered as the proper medication for a patient?
(A) For dry and irritating coughs that do not involve mucus production.
(B) Non-productive cough
38
What are some side effects of antitussives?
(A) Drowsiness
(B) Dizziness
(C) Nausea
39
What are some contraindications and cautions of antitussives?
Should not usually be used for an ongoing cough from smoking or long term breathing problems (such as chronic bronchitis and emphysema) unless directed medically.
40
What are some examples of antitussives
(A) Dextromethorphann hydrobromide (Benylin)
(B) Butamirate (Sinecod)
41
What is the mechanism of action of expectorants?
(A) Decrease surface tension of secretions by reducing viscosity
(B) Increasing the water content of secretions which decreases their viscosity (bronchial secretion enhancers)
(C) Dissolving the chemical bonds within the secretions, causing them to thin (mucolytics)
42
These medications are used to relieve chest congestion that occurs because of a cold, the flu or allergies.
Expectorants
43
What are some side effects of expectorants?
Drowsiness, nausea and vomiting
44
Based on the categories of asthma medications, what are the different acute relief medications?
(A) Short-acting beta antagonist (SABA)
(B) Systemic corticosteroids
(C) Anticholinergics
45
Based on the categories of asthma medications, what are the different long-term controlled medications?
(A) Inhaled corticosteroids
(B) Long-acting beta-2 Agonist (LABA and ultra-LABA)_
(C) Mast cell stabilizers
(D) Methylxanthins
(E) Leukotriene modifiers
(F) Anti-IgE antibodies
46
Based on the categories of asthma medications, what are the different added (miscellaneous) medications?
Sympathomimetics
47
These are the first line medications for acute treatment in asthma symptoms and exacerbations.
Short-acting Beta-2 Antagonists
48
Short-acting Beta-2 Antagonists (SABA) are often used in conjunction with what:
(A) LABAs
(B) Inhaled corticosteroids
(C) Long-acting muscarinic agonists in treatment for COPD
49
What is the typical administration of Short-acting Beta-2 Antagonists?
Inhalation via metered dosing or dry powder inhalation
50
Why is the inhalation route preferred over the alternative oral administration when administering Short-acting Beta-2 Antagonists?
Because inhalation has an increase in therapeutic value and a decrease in systemic side effects.
51
What are the common examples of Short-acting Beta-2 Antagonists (SABAs)?
(A) Salbutamol (Ventolin)
(B) Terbutaline (Bricanyl)
52
This medication is known as the "hallmark SABA."
Salbutamol (Ventolin)
53
What is the onset action and the therapeutic effect duration of Salbutamol?
Onset of Action: Under 5 minutes
Therapeutic Effect Duration: Between 3 to 6 hours
54
What is the half-life of Salbutamol?
2.7 or 5 hours
55
Aside from being commonly used as an airway treatment (acute exacerbation of asthma and/or COPD), nebulized salbutamol is also useful for?
Useful as a treatment for hyperkalemia by providing a rapid shift of intracellular potassium.
56
This is a commonly used short-acting beta-2 agonist as a tocolytic in the cessation of labor contractions.
Terbutaline
57
What is the half-life of terbutaline?
16 hours
58
What is the mechanism of action of Short-acting Beta-2 Antagonists?
The B2-adreneceptor agonist (light green) binds to the B2 receptor (purple), which activates the adenyl cyclase, resulting in the conversion of ATP to cyclic AMP (cAMP). This promotes bronchodilation and relieves symptoms experienced during an acute asthma episode.
59
What are indications of Short-acting Beta-2 Antagonists?
(A) It provides symptomatic relief and prevention of bronchospasm due to bronchial asthma, chronic bronchitis, reversible obstructive airway disease, and other chronic bronchopulmonary disorders (COPD), in which bronchospasm is a complicating factor.
(B) It also prevents acute prophylaxis against exercise-induced bronchospasm and other stimuli known to induce bronchospasm.
60
Salbutamol for acute bronchospasm, administered via inhalation, is used to treat and prevent what?
Treatment and prevention in patient with reversible obstructive airway disease.
61
How is salbutamol administered as a metered dose-aerosol or dry powder inhaler (90 or 100 mg/actuation) - for acute bronchospasm?
Administered with 1 to 2 inhalations every 4 to 6 hours with a maximum of 800 mcg daily
62
How is salbutamol administered as a metered dose-aerosol or dry powder inhaler (90 or 100 mg/actuation) - for exercise-induced bronchospasm?
Administered with 2 inhalations every 15 to 30 minutes prior to exercise.
63
How is Salbutamol administered for acute bronchospasm in adults?
Through inhalation or nebulization.
64
What is the recommended dosage of Salbutamol for adults during acute bronchospasm?
2.5 to 5 mg (1.25 to 2.5 ml) per nebulization.
65
How often can Salbutamol nebulization be repeated if necessary?
Every 20 to 30 minutes.
66
What is the concentration of Salbutamol in the solution for inhalation?
2 mg/ml.
67
How much Salbutamol does a unit dose vial contain?
5 mg of Salbutamol in 2.5 ml of solution.
68
Can Salbutamol be diluted before nebulization?
Yes, it may be diluted with normal saline solution (NSS) in a 1:1 ratio to increase aerosolization.
69
What is the dosage of Salbutamol for severe bronchospasm when administered intravenously?
250 mcg (4 mcg/kg) as a 50 mcg/mL solution.
70
Can the IV dose of Salbutamol for severe bronchospasm be repeated?
Yes, it may be repeated if necessary.
71
What is the usual infusion rate for Salbutamol when given as a 10 mcg/mL solution?
The usual rate is 3 to 20 mcg/min, adjusted according to the patient’s needs.
72
How is Salbutamol prepared for IV injection?
Dilute an ampoule containing 500 mcg/mL with 10 mL of water for injection to make a solution of 50 mcg/mL.
73
How is Salbutamol prepared for IV infusion?
Dilute 5 mL of Salbutamol injection with 500 mL of normal saline (NaCl) or dextrose injection to create a concentration of 10 mcg/mL.
74
What is the parenteral dose of Salbutamol for severe bronchospasm in adults?
50 mcg via subcutaneous (SC) or intramuscular (IM) injection, given every 4 hours as required.
74
How often can Salbutamol be administered via SC or IM injection for severe bronchospasm?
Every 4 hours, as needed
75
What is the dosage of Salbutamol for bronchospasm when taken as an oral syrup or immediate-release tablet?
2 to 4 mg, 3 to 4 times daily, which may be increased up to a maximum of 8 mg 3 to 4 times daily, as tolerated.
76
What is the dosage of Salbutamol for bronchospasm when taken as an extended-release tablet?
4 to 8 mg, taken every 12 hours.
77
What is the initial oral dose of Salbutamol for elderly patients when using the syrup or immediate-release tablet?
2 mg, taken 3 or 4 times daily.
78
What type of receptor does Salbutamol selectively target?
Beta-2 adrenergic receptors, which are abundant on airway smooth muscle cells.
78
What intracellular process does Salbutamol activate upon binding to beta-2 receptors?
It increases the formation of intracellular cAMP by stimulating adenylyl cyclase.
79
What happens when salbutamol increases the formation of intracellular cAMP by stimulating adenylyl cyclase?
(A) Relaxes airway smooth muscle (bronchodilation)
(B) Inhibits release of bronchoconstricting mediators from mast cells.
(C) Inhibits microvascular leakage
(D) Increases mucociliary transport
80
What are the principal routes of administration for Salbutamol?
The principal routes are inhaled or intravenous (IV). It can also be given orally (PO), subcutaneously (SC), or intramuscularly (IM), though less commonly.
81
How is Salbutamol absorbed in the body?
the gastrointestinal tract (GIT) and the lungs.
82
When are the effects of inhaled Salbutamol maximal?
The effects are maximal 15-30 minutes post-administration.
83
How long do the effects of inhaled Salbutamol last?
The effects persist for 3 to 6 hours.
84
Is Salbutamol metabolized in the lungs?
No, there is no metabolism of Salbutamol in the lungs.
85
What percentage of Salbutamol undergoes first-pass metabolism?
50% of Salbutamol undergoes first-pass metabolism.
86
How is Salbutamol metabolized in the liver?
It is sulphated in the liver to form inactive metabolites.
87
Does Salbutamol strongly bind to plasma proteins?
No, it is weakly bound to plasma proteins.
88
Where does Salbutamol primarily act when administered via inhalation?
It acts topically on the bronchial smooth muscle.
89
Is Salbutamol detectable in the blood immediately after inhalation?
No, it is initially undetectable in the blood.
90
When do low concentrations of Salbutamol appear in the blood after inhalation?
After 2 to 3 hours, low concentrations are seen, likely from the portion of the dose that is swallowed and absorbed in the gut.
91
Are systemic levels of Salbutamol high after inhaling recommended doses?
No, systemic levels of Salbutamol are low after inhalation of recommended doses.
92
What are the two common formulations of Salbutamol for inhalation therapy?
Nebulized Salbutamol and Spacer/Inhaler.
92
What is an advantage of using nebulized Salbutamol?
No patient education is required, and it avoids first-pass metabolism.
93
What is a disadvantage of using nebulized Salbutamol?
Larger particles require a higher dose, and there is a higher incidence of systemic side effects.
94
What is an advantage of using a spacer/inhaler with Salbutamol?
It is as effective as nebulized Salbutamol when used properly, can be used at a lower dose, has fewer side effects, and also avoids first-pass metabolism.
95
What is a disadvantage of using a spacer/inhaler for Salbutamol?
Patient education is required to use it effectively.
96
What causes the adverse effects of Salbutamol
The adverse effects are related to the stimulation of beta-2 receptors, which are located in skeletal muscle, vascular and bronchial smooth muscle, the liver, and on cell membranes.
97
What musculoskeletal adverse effect is commonly associated with Salbutamol?
(A) Tremors due to stimulation of beta-2 receptors in skeletal muscle.
98
What cardiovascular adverse effects can Salbutamol cause?
(A) Tachycardia
(B) Palpitations
(C) Arrhythmias
99
What is the mechanism behind Salbutamol’s cardiovascular adverse effects?
It involves direct stimulation of atrial beta-2 receptors and peripheral vasodilation, which leads to reflex cardiac stimulation.
100
What respiratory adverse effect can Salbutamol cause?
Ventilation-perfusion (V/Q) mismatch and a transient decrease in PaO2.
101
Why does Salbutamol cause a transient decrease in PaO2?
The vasodilatory action of the beta-2 agonist increases perfusion of poorly ventilated lung units, leading to a temporary drop in oxygen levels (PaO2).
102
What metabolic adverse effect is commonly associated with Salbutamol?
Hypokalemia, due to the entry of potassium into skeletal muscle.
103
What systemic metabolic effects can occur with large systemic doses of Salbutamol?
An increase in free fatty acids (FFA), insulin, glucose, pyruvate, and lactate, though these are generally only seen with large doses.
104
Is lactic acidosis common with Salbutamol use?
No, lactic acidosis is rare.
105
What gastrointestinal adverse effect can Salbutamol cause?
Vomiting.
106
What are the monitoring parameters for salbutamol?
(A) Peak flow, and/or other pulmonary function tests
(B) Blood pressure, heart rate, CNS stimulation
(C) Serum glucose, Vitamin K and Creatinine
(D) Asthma symptoms
(E) Arterial or capillary blood gases if needed
(F) Lactate
(G) ECG (IV)
107
What is the risk of hypokalemia associated with Salbutamol when used with other medications?
There is an increased risk of hypokalemia when used with corticosteroids, diuretics (e.g., loop, thiazide), and xanthines (e.g., theophylline).
108
What effect do MAO inhibitors and tricyclic antidepressants (TCAs) have when combined with Salbutamol?
They increase vascular effects when used with Salbutamol.
109
What is the consequence of using beta-blockers (e.g., propranolol) with Salbutamol?
It may cause severe bronchospasm.
110
How can Salbutamol affect digoxin levels?
Salbutamol may decrease serum concentrations of digoxin.
111
What is the first step in managing Salbutamol overdosage?
Symptomatic treatment and monitoring serum potassium (K) and lactate levels.
112
Can a beta-blocker be used in cases of Salbutamol overdosage?
Yes, a cardioselective beta-blocker may be given with caution.
113
What treatment may be administered for hypokalemia in Salbutamol overdosage?
Oral or intravenous potassium may be given as needed.
114
How do the effects of glucocorticoids vary with dosage?
The anti-inflammatory and immunosuppressive effects are dose-dependent, with immunosuppressive effects primarily seen at higher doses.
115
What are the two types of mechanisms through which glucocorticoids exert their pharmacological effects?
(A) Genomic mechanisms
(B) Non-genomic mechanisms
116
These medications inhibit genes responsible for the expression of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and pro-inflammatory cytokines such as tumor necrosis factor alpha and various interleukins.
Corticosteroids
117
What proteins do corticosteroids regulate to reduce inflammation?
They initiate the regulation of lipocortin and annexin A1, which reduce prostaglandin and leukotriene synthesis and inhibit COX-2 activity.
117
How do corticosteroids affect neutrophil migration?
They reduce neutrophil migration to inflammatory sites.
118
Why do corticosteroid effects persist even when they are no longer detectable in plasma?
Because their action occurs intracellularly, leading to prolonged effects even after plasma detection is absent.
119
What are the currently recommended systemic steroids for moderate to severe asthma exacerbations?
Oral prednisone and dexamethasone.
120
What are some parenteral formulations of systemic corticosteroids?
Hydrocortisone and methylprednisolone.
121
How do the oral and parenteral routes of corticosteroid administration compare in effectiveness?
Studies have found both routes to be equally effective, with the oral route being less painful and invasive.
122
What is the typical dosing schedule for prednisone in asthma exacerbations?
Prednisone is given for 5 days at a dose of 1 to 2 mg/kg daily (maximum 50 mg/day).
122
What is the half-life of prednisone?
The half-life of prednisone is 18 to 36 hours.
123
How is dexamethasone administered for asthma exacerbations?
Dexamethasone can be given for 1 to 5 days at a dose ranging from 0.3 to 0.6 mg/kg daily.
124
What is the half-life and potency of dexamethasone compared to prednisone?
Dexamethasone is a long-acting glucocorticoid with a half-life of 36 to 72 hours and is 6 times more potent than prednisone.
125
What did studies find regarding short bursts of prednisone (1-2 mg/kg daily for 5 days) and their impact on bone density, height, and adrenal function?
No effect was observed on bone density, height, and adrenal function at 30 days, but transient decreases in bone deposition and adrenal function were noted.
125
What are some short-term effects of systemic corticosteroids?
Short-term effects include hyperglycemia, disturbances of blood pressure, edema, gastrointestinal bleeding, psychiatric problems, poor wound healing, increased risk of infection, and electrolyte disorders (hypokalemia and hyperkalemia).
126
What factors influence the risk of adverse effects from corticosteroid therapy?
The risk is related to the dose, duration of therapy, and the specific agent used.
127
What are the different nursing implications for systemic corticosteroids?
(A) Establish baseline and continuing data on BP, weight, fluid and electrolyte balance, and blood glucose.
(B) Lab tests: Periodic serum electrolytes blood glucose, Hct and Hgb, platelet count, and WBC with differential.
(C) Monitor for adverse effects. Older adults and patients with low serum albumin are especially susceptible to adverse effects.
(D) Be alert to signs of hypocalcemia
128
What are the different LONG TERM nursing implications for systemic corticosteroids?
(A) Monitor for persistent backache or chest pain; compression and spontaneous fractures of long bones and vertebrae present hazards.
(B) Monitor for and report changes ni mood and behavior, emotional instability, or psychomotor activity, especially with long-term therapy.
129
What should be noted regarding dose adjustments for patients on corticosteroids?
Dose adjustment may be required if the patient is subjected to severe stress, such as serious infection, surgery, or injury.
129
What should nurses be alert for when administering systemic corticosteroids?
Nurses should be alert to the possibility of masked infections and delayed healing due to the anti-inflammatory and immunosuppressive actions of corticosteroids.
130
Do single doses or short-term use of corticosteroids (<1 week) produce withdrawal symptoms upon discontinuation?
No, single doses or short-term use of corticosteroids do not produce withdrawal symptoms, even with moderately large doses.
131
What should be taught to the patient and their family regarding systemic corticosteroids?
(A) Expect a slight weight gain with improved appetite.
(B) Avoid alcohol and caffeine; may contribute to steroid-ulcer development in long-term therapy.
(C) Do not ignore dyspepsia with hyperacidity. Report symptoms to physician and do not self-medicate to find relief.
(D) Do NOT use aspirin or other OTC drugs unless prescribed specifically by the physician.
(E) A high protein, calcium, and vitamin Diet is advisable to reduce risk of corticosteroid-induced osteoporosis.
(F) Notify physician of slow healing, any vague feeling of being sick, or return to pretreatment symptoms.
(G) Do not abruptly discontinue drug; doses are gradually reduced to prevent withdrawal symptoms.
(H) Report exacerbation of disease during drug withdrawal.
(I) Carry medical identification at al times. It needs to indicate medical diagnosis, drug therapy, and name of physician.
(J) Do not breast feed while taking/using this drug without consulting physician.
132
This is a quaternary ammonium derivative of atropine and acts as an anticholinergic agent.
Ipratropium
133
How is Ipratropium commonly administered, and why?
It is commonly administered through inhalation to produce a local effect with minimal systemic absorption.
134
In what condition is inhaled Ipratropium indicated when used in combination with inhaled beta-agonists and systemic corticosteroids?
It is indicated for the management of severe asthma exacerbations requiring treatment.
135
What chronic condition is Ipratropium indicated for as a bronchodilator?
For the maintenance treatment of bronchospasm associated with chronic obstructive pulmonary disease (COPD), including chronic bronchitis and emphysema.
136
What is the recommended dosage for Ipratropium when administered as a metered-dose aerosol for asthma or COPD?
The recommended dosage is 20-40 mcg, 3-4 times daily. Single doses of up to 80 mcg may be required for some patients.
137
What is the recommended dosage for Ipratropium when administered as a solution for nebulization?
The recommended dosage is 250-500 mcg, 3-4 times daily.
138
How does Ipratropium bromide cause bronchodilation?
Ipratropium bromide causes bronchodilation by blocking the action of acetylcholine at parasympathetic sites in bronchial smooth muscle.
139
How does Ipratropium work to produce bronchodilation?
Ipratropium inhibits the parasympathetic nervous system at the level of the airway, resulting in bronchodilation.
140
What is the onset of bronchodilation when using Ipratropium?
The onset of bronchodilation occurs within 15 minutes.
141
How long does the effect of Ipratropium last after administration?
The effect begins after 1-2 hours and lasts for 4 to 6 hours.
142
How well is Ipratropium absorbed when administered orally or by inhalation?
Ipratropium is poorly absorbed, with serum levels corresponding to only 1-2% of the administered dose.
143
What percentage of a dose of Ipratropium is deposited in the lungs?
Approximately 10-30% of the administered dose is deposited in the lungs, while a small amount reaches systemic circulation.
144
How well is Ipratropium absorbed from the gastrointestinal (GI) tract?
Ipratropium is poorly absorbed from the GI tract.
145
When is the peak concentration of Ipratropium reached after administration?
The peak concentration is reached after 1-2 hours.
146
What is the bioavailability of Ipratropium when administered via oral inhalation and nasal routes?
The bioavailability is 2% for oral inhalation and 7-28% for nasal administration.
147
How is Ipratropium metabolized in the body?
Ipratropium is metabolized via ester hydrolysis (41%) and conjugation (36%).
148
How is Ipratropium distributed in the body?
Ipratropium is highly distributed in the tissues, but the circulating levels of the drug are very minimal.
149
What percentage of Ipratropium is in a bound state after oral inhalation and nasal administration?
After oral inhalation, only 0-9% of the dose is in a bound state, and less than 20% for nasal administration.
150
How is Ipratropium eliminated from the body?
Ipratropium is primarily eliminated via urine (80-100%) and to a lesser extent through feces (less than 20%).
151
What happens to Ipratropium in the urine after elimination?
Almost all of the drug found in the urine is unchanged.
152
What is the half-life of Ipratropium for oral inhalation and nasal administration?
The half-life is 2 hours for oral inhalation and 1.6 hours for nasal administration.
153
What are some common adverse effects of Ipratropium?
Common adverse effects include dry mouth, constipation, tachycardia, palpitations, arrhythmias, nausea, vomiting, and dyspepsia.
154
What ocular complications can occur with Ipratropium?
Ocular complications can include mydriasis and narrow-angle glaucoma.
155
What are some rare but serious adverse effects of Ipratropium?
Rare adverse effects include urinary retention, hypersensitivity reactions (e.g., urticaria, angioedema, rash), nasal dryness, irritation, and epistaxis.
156
What potentially fatal adverse effects can occur with Ipratropium use?
Potentially fatal adverse effects include paradoxical bronchospasm and anaphylaxis.
157
What are the precautions that one should take note of when administering ipratropium?
(A) PREGNANCY CATEGORY B:
Inhalation/Respiratory/Nasal
(B) Pregnancy and lactation
(C) Patient w/ prostatic hyperplasia/bladder neck obstruction
(D) Myasthenia gravis
(E) Narrow-angle glaucoma cystic fibrosis
158
What are the contraindications for using Ipratropium?
Ipratropium is contraindicated in patients with hypersensitivity to ipratropium, atropine, or their derivatives.
159
What drug interactions should be noted when using Ipratropium?
Ipratropium has an additive bronchodilatory effect when used with β-adrenergic drugs and xanthine preparations.
160
What important advice should be given to patients using Ipratropium?
Patients should be informed that this drug may cause dizziness, accommodation disorder, mydriasis, and blurred vision. If affected, they should avoid driving or operating machinery.
161
What is the initial management for mild to moderate Ipratropium overdose?
For mild to moderate cases, the dose should be reduced.
162
What should be monitored in severe cases of Ipratropium overdose?
In severe cases, monitor acid-base balance, blood sugar, electrolyte levels, blood pressure, heart rate, and rhythm. Correct any metabolic changes.
163
What drug may be used with caution for arrhythmias in Ipratropium overdose?
A cardioselective β-blocker, such as metoprolol, may be used with caution to treat arrhythmias.
