Respiratory System Affecting Agents Flashcards
(118 cards)
1
Q
Beta 2 adrenoreceptor agonist
A
Short acting ( SABA)-Salbutamol
Long acting ( (LABA)-Formoterol
2
Q
Glucocorticosteroids inhaled(IGC)
A
Fluticasone, Budesonide
3
Q
Systemic glucocorticosteroids
A
Prednisolone
4
Q
M cholinoreceptor antagonists
A
Short acting ( SAMA)- ipratropium
Long acting ( LAMA)-Tiotropium
5
Q
Phosphodiesterase inhibitor (PDE)
A
Roflumilast
6
Q
Anti IgE
A
Omalizumab
7
Q
Anti IL 5 R
A
Benralizumab
8
Q
Leukotriene receptor antagonist
A
Montelucast
9
Q
Anti cough agents
A
Codeine ,dexyromethorphan
10
Q
Mucolytic agent
A
Acetylcysteine
11
Q
Antihistamines (H1 RA)
A
Clemastine,Loratadine,cetrizine,azelastine
12
Q
A
13
Q
Cromones
A
Sodium cromoglycate
14
Q
Decongestants
A
Xylometazoline, pseudoephedrine
15
Q
COPD
A
Persistent airway obstruction, progressive,young people and children doesn’t have COPD
16
Q
COPD risk factor
A
Smoking and age
17
Q
3 most common causes of cough
A
Bronchial asthma, reflux disease,nasal drip syndrome in rhinitis
18
Q
Since cough is a vital reflex,purpose of treatment is
A
To restore normal cough reflex
19
Q
Chronic cough duration
A
Lasting for more than 8 weeks
20
Q
Allergic rhinitis
A
Allergen induced inflammation of nasal mucosa by IgE mediated reaction to one or more allergens
21
Q
Treatment of allergic rhinitis.like asthma has 3 imp elements:
A
Control of environmental factors, avoidance of allergens, pharmacotherapy and immunotherapy
22
Q
Asthma
A
Chronic airway inflammation with variable airway obstruction and cause respiratory hyperreactivity
23
Q
Consequence of asthma is
A
Potential narrowing of airways ( bronchospasm) in form of shortness of breath ( asthma attack)
24
Q
Asthma attack can be caused by
A
Absolutely harmless irritants like cold air,dust, exercise, medication etc
25
Asthma is characterized by ---- airway obstruction, while COPD -------airway obstruction
Reversible airway obstruction, incomplete reversible obstruction
26
First line agents in asthma management
Inhaled Glucocorticoid
27
Second imp pharmaco group which is used in asthma management
Inhaled bronchodilators
28
In long-term asthma structural changes happens like:
Epithelial shedding,thickening of BM( subepithelial fibrosis), angiogenesis, hyperplasia of mucus secreting cells,smooth muscle hypertrophy and hyperplasia
29
In late phase response to allergen exposure --- happens
Recruitment of multiple subtypes of immune cells like eosinophil, neutrophil, memory T cell
30
In severe case of asthma release of multiple inflammatory mediators can cause
Cholinergic hyperreactivity that increase both mucus secretion and bronchoconstriction - can be reduced by inhaled anti muscarinic
31
For asthma attacks ( exacerbations) therapy
SABA,LABA
32
For Control therapy for asthma ,use
Antiinflammatory agents-Glucocorticoids( I or S), Leukotriene receptor antagonist
Bronchodilators - LABA,M cholinoblockers
Targeted therapy - Anti- IgE,Anti-IL5R
33
Inhaled corticosteroids ( IGC) - Fluticasone, Budesonide. , action
Inhibition of phospholipase A2,inhibition of prostaglandin and leukotriene synthesis, Restoration of beta adrenoreceptor sensitivity
34
Clinical use of fluticasone and Budesonide ( inhaled corticosteroids)
Asthma control therapy, allergic rhinitis,COPD
35
For allergic rhinitis use
Glucocorticosteroids nasal
36
Fixed combination of LABA and IGC medications used for inhalation
Formoterol + Budesonide
37
SE of inhaled corticosteroids
Mouth fungal infection ( candidiasis),Risk of cataract,risk of osteoporosis.
Oral hygiene after IGC imp
Risk of systemic SE increase with high dose of IGC
38
Systemic glucocorticosteroids ( prednisolone) use
Severe asthma exacerbations (p/o or I/v)
39
Leukotriene receptor antagonist (LTRA) - Montelukast action
Decrease bronchoconstriction,anti allergic,anti inflammatory effect,improves IGC efficiency,As a reserve for aspirin, exercise induced asthma, allergic rhinitis
40
Leukotriene is a
Proasthmatic biologically active substance
41
Clinical use of leukotriene receptor antagonist ( Montelukast)
Prevention of asthma attacks, allergic rhinitis
42
Stimulation of beta 2 adrenoreceptor in bronchial smooth muscle ends cause
Bronchodilation
43
Formoterol compared to other LABA has
Long duration of action,but faster onset of action
44
SABA( salbutamol/albuterol) onset of action and duration
3-5 min, duration:4 to 6 hrs
45
Clinical use of SABA( salbutamol and albuterol)
Bronchospasm therapy and prevention
46
LABA(Formoterol) onset and duration
3 min, duration 12-16 hr
47
LABA( Formoterol) ise
Asthma control therapy,COPD
48
SE of bronchodilators ( SABA and LABA)
Tachycardia,tremor, hypokalemia
49
M cholinoreceptor antagonist
SAMA- ipratropium
LAMA-Tiotropium
50
M cholinoreceptor antagonist ( SAMA- ipratropium,LAMA- Tiotropium) action
M 1-3 cholinoreceptor antagonist, bronchodilator, anti secretory action
51
Clinical use of M cholinoreceptor antagonist ( Ipratropium, Tiotropium)
COPD, Bronchial, allergic rhinitis ( ipratropium nasal)
52
Bronchodilators ( M cholinoreceptor antagonist ( ipratropium and Tiotropium) side effect
Dry mouth, mydriasis
53
Precautions for choline for patients withblockers use
Glaucoma, prostate hyperplasia, bowel atony
54
Anticholinergics inhibits --- nerve tone in airways
N.vagus( leading to bronchodilation)
55
56
57
M cholinoblockers have higher effect on ----- caliber bronchi compared to beta 2 agonists
Large caliber
58
Beta 2 agonists have higher effect on
Small caliber bronchi
59
Inhalation therapy distribution depends on
Particle size and efficacy of delivery method
60
Most inhaled drugs get swallowed and undergo
First pass effect and some enters systemic circulation from lungs
61
To reduce systemic effect of inhalers use
Large volume spacer
62
Types of inhalers
Dosed aerosols, powder inhaler,fogger or nebulizer
63
Phosphodiesterase inhibitor ( Roflumilast) action
Selective PDE 4 inhibition, inactivate transcription factor involved in inflammatory process( use CAMP- PKA pathway)
Direct antiinflammatory effect
Indirect bronchodilator effect
64
Clinical use of Roflumilast ( phosphodiesterase inhibitor)
Severe forms of COPD
65
PDE 4 is
Dominant type of PDE in lung immune competent cells( eg: macrophages, neutrophil)
66
Anti IgE( Omalizumab) ( anti allergic effect)use
Severe persistent IgE mediated asthma
67
Anti IgE bind to
Ce3 domain of circulating I gE, prevent their binding to receptor on mast cells and lymphocyte - stops allergic cascade
68
Anti IL5 ( Benralizumab) action
Blocks eosinophil IL 5 receptor, cause cell induced cytotoxicity and induce apoptosis
69
Clinical use of benralizumab ( Anti IL5
Severe eosinophil asthma that is not controlled with IGC / LABA
70
Combinations used in COPD
SAMA +SABA-iprqtropium + formoterol
LAMA + LABA
71
If COPD is eosinophilia, antiinflammatory therapy with ---+ is done
Inhaled Glucocorticoid
72
H1 receptor action
Increase Ip3 and Calcium,in bronchi - bronchoconstriction,in BV- vasodilation, capillary wall permeability increase,in nervous system - irritation of sensory nerves- itching
73
H2 receptor action
Increase adenylate cyclase and camp,in stomach - increase HCl secretion,in BV- vasodilation and increase capillary wall permeability
74
H3 receptor action
Decrease adenylate cyclase and CAMF,in CNS cause modulation of histamine release,in BV - vasodilation
75
1 st gen H1RA( clemastine )action
Blocks central and peripheral H1 receptor, reduce itching ( antiallergic),
Cholinoblocking effect ( central cholinoblocking - antiemetic effect)
76
Clinical use of clemastine ( H1RA)
Allergic rhinitis,Hives, Allergic skin conditions such as atopic dermatitis
77
SE of clemastine ( H1RA)
Sedation, drowsiness,dry mouth, urinary retention
78
Depending on dose on CNS by clemastine induce
Agitation
79
1 st gen H1RA
Clemastine
80
Interactions of 1 st gen H1RA clemastine
Enhance sedative effect of alcohol,CNS depressant, effect of anticholinergic drugs( atropine, tricyclic antidepressants)
81
1 st gen H1RA clemastine is often combined with
Antipyretic/ analgesic to treat common cold
82
Driving while using H1RA is
Not recommended
83
2 Nd gen H1 RA
Azelastine, Loratadine, cetrizine
84
2 Nd gen H1RA action
Selective peripheral H1 receptor blockade, reduce itching, stabilise mast cells( anti allergic effect)
85
Cetrizine and Loratadine are not
Lipophilic so doesn't cross BBB
86
Azelastine is used in
Topical dosage forms( nasal drip,eye drops etc)
87
Clinical use of 2 Nd gen H1RA
Allergic rhinitis,Hives, allergic conjunctivitis
88
Toxicity by H1 RA symptoms
Decrease consciousness, irritability, hallucinations, seizures, Typical anticholinergic symptoms: dry mouth, mydriasis, Tachycardia, facial hyperemia, GI disorders
89
Treatment of histamine toxicity
Symptomatic
90
Degranulation inhibitors ( antihistamine)
Sodium cromoglycate
91
Sodium cromoglycate is a
Eye drops,blocks calcium channel in mast cells - inhibit their degranulation,prevents histamine release. (Antiallergic effect)
92
Sodium cromoglycate ( degranulation inhibitors) use
Allergic rhino conjunctivitis
93
Alpha adrenoreceptor agonist ( nasal decongestant eg:
Xylometazoline
94
Xylometazoline ( alpha adrenoreceptor agonist) nasal decongestant action
Local stimulation of alpha 1 and 2 adrenoreceptor - reduce mucosal edema and has vasoconstrictive effect
95
Why shouldn't we use xylometazoline more than 7 days
It cause rhinitis medicamentosa- secondary vasodilation.Prolonged or excessive use cause repeated nasal congestion and or atrophy of nasal mucosa
96
Overdose with xylometazoline ( decongestant) can cause
Increase BP
97
Clinical use of xylometazoline ( alpha adrenoreceptor agonist)
Acute ( allergic, vasomotor) rhinitis
98
Pseudoephedrine ( decongestant) is a
Active sympathomimetic amine,alpha adrenomimetics activity more than beta.peroral use
Vasoconstrictive effect, indirect sympathomimetic effect
99
Clinical use of pseudoephedrine ( decongestant)
Acute allergic vasomotor rhinitis
100
Pseudoephedrine is a stereoisomer of
Ephedrine and has weaker vasoconstrictive effect that ephedrine and less effects on CNS
101
Pseudoephedrine is not used alone and overdose may cause
Sympathomimetic symptoms likes insomnia, anxiety, agitation
102
Sympathomimetic decongestant can cause
Sympathomimetic toxidrome and excessive vasoconstriction cause multi organ damage
103
Pseudoephedrine is sometimes used as
Narcotics off lebel
104
Pseudoephedrine toxidrome disappears mostly within
4 to 6 hrs
105
Main symptoms of pseudoephedrine toxicity
Hypertension , Tachycardia, headache,confusion,tremors, mydriasis, urinary disturbance, seizures, intracranial hemorrhage
May also cause: insomnia, anxiety, agitation
106
Decongestants should be used with caution in patients with
Hypertension,CHD, Hyperthyroidism,BPH
107
Anti cough agents( central acting antitussive) action - codeine
Suoress medulla oblongata cough center,mu opioid receptor agonists - anti cough effect and poor analgesic effect
108
Clinical use of codeine ( munopioid receptor agonist
Dry,non productive cough
109
SE of codeine ( mu opioid receptor agonists)
Constipation
( May cause respiratory depression and addiction)
110
Dextromethorphan ( central action antitussive) action
Sigma 1: receptor agonists,NMDA receptor antagonist
Anti cough effect
111
Clinical use of dextromethorphan
Dry,non productive cough
112
SE of dextromethorphan ( antitussive)
Drowsiness
Overdose cause euphoria, children and seniors hallucinations, addiction
113
Acetylcysteine ( mucolytic agent) action
Depolymerization of mucoprotein,secretolytic effect),restore glutathione amount in liver
114
Clinical use of acetylcysteine ( mucolytic agent)
Acute/ chronic bronchitis with sputum excretion problems and paracetamol intoxication
115
Interactions of acetylcysteine ( mucolytic agent)
Antibiotic inactivation - use with 2 HR interval
116
Contraindications of acetylcysteine
Acute gastric ulcer
117
Dry non productive cough treatment options
Dextromethorphan and codeine
118
Acute allergic rhinitis treatment
Pseudoephedrine and xylometazoline
