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Respiratory Module > Pharmacology asthma COPD > Flashcards

Pharmacology asthma COPD Flashcards

1
Q

Asthma

A

Inflammatory condition with recurrent reversible airway obstruction due to stimuli too weak to affect non asthmatic people

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2
Q

Symptoms of asthma

A

Wheezing
Shortness of breath especially breathing out
Cough sometimes

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3
Q

Difference between asthma and COPD

A

In asthma , airway obstruction is reversible

COPD , obstruction not reversible or partially reversible

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4
Q

Status asthmaticus

A

Acute severe asthma which is not easily reversible and can cause hypoxemia which requires hospitalization because fatal

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5
Q

Asthma 3 characteristics

A

Bronchial hyperactivity

Reversible broncho constriction

Airways inflammation

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6
Q

Immediate phase of asthma

A

Stimulus binds and activate mast cell

Mast cells release spasm ovens (cysLTs, histamine and PGD2) —> bronchospasm

Mast cells release chemotaxins and chemokines which lead to late phase

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7
Q

Drugs classes that can revert bronchospams effet in immediate phase

A

B2 adrenoreceptors agonists

CystLT receptor antagonists

Theophylline

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8
Q

Late phase of asthma

A

Infiltration of cytokines

Release of Th2 cells , monocytes

Activation of inflammatory cells specially eosinophils

Release of mediatiors (cysLTs, neuropeptides, NO, adenosine) and EMBO, ECP ( cause epithelial damage) —> airway inflammation and hyper reactivity —-> bronchospam, wheezing, coughing

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9
Q

Drugs that can act in late phase of asthma

A

Glucocorticoids

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10
Q

Drug therapy for asthma

A

Bronchidilators ( reverse brinchospam)

Anti inflammatory agent (prevent or inhibit inflammation)

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11
Q

Types of bronchodilators

A

B2 adreno receptors agonists

Xanthines

Cysteinyl Leukotriene receptor antagonists

Muscarinic receptor antagonists

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12
Q

Effect of B adrenoreceptor agonist

A

Dilate bronchi by direct action On smooth muscle no matter stimulus

Inhibit mediator release from mast cells
Inhibit TNF à release from monocytes
Increase mucus clearance by cilia action

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13
Q

Mode of administration of b adrenoreceptor agonists

A 
Inhalation (metered dose inhaler ) oral 
Powder 
Nébulisation 
Orally 
Injection
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14
Q

B adrenoreceptor agonists short acting

A

Inhalation :

Salbutamol 
Terbutaline
Metaproterenol 
Levalbuterol 
Pirbuterol
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15
Q

Short acting b adrenorefeotor agonist duration of action

A

3-5h so used on “as needed” basis

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16
Q

Long acting b adrenoreceptor agonist

A

Inhalation:

Salmeterol
Formoterol
Vilanterol

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17
Q

Long acting b adrenorefeotor agonist duration of action

A

8-12h

Given regularly twice daily when asthma of patient inadequately controlled by glucocorticoids

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18
Q

B adrenoreceptor agonist combination

A

Albuterol + ipratropium

Salmeterol+ fluticasone

Formoterol+ moments some

Formoterol + budesonide

Vilanterol + fluticasone

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19
Q

B adrenoreceptor agonist unwanted effects

A

Tremor
Tachycardia
Cardiac dysrhythmia

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20
Q

Xanthines agents

A

Theophylline

Aminophylline

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21
Q

Xanthine action

A

Relaxant effect on smooth muscle by inhibit phosphodiestarase isoenzymes -> Increase in cAMP

Antiinflammatory action by inhibit type IV phosphodiesterase which is involved in inflammation

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22
Q

Theophylline interaction with glucocorticoid

A

Activates histone deacetylase so can reverse resistance to anti inflammatory effect of corticosteroids

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23
Q

Methylxanthine impact on CNS and respiratory system

A

Stimulate it so can be beneficial in COPD patients with reduced respiration with CO2 retention

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24
Q

Therapeutic index of theophylline

A

Narrow 30-100 micromol

Adverse effect at 110

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25
Side effects of theophylline
Act on CNS CVS GI diuresis | Cause insomnia , nervousness etc
26
What happens when xanthines concentration goes above 200
Serious CVS and CNS effects Dysrhythmias which can be fatal Seizures (fatal if respiration impaired )
27
Theophylline mode of administrion
Oral sustained release préparation
28
Aminophylline mode of administration
Slow IV of loading dose And then IV infusion
29
Theophylline absorbed by
GIT
30
Metabolism of theophylline
p450 metabolism Induced by smoking , so less duration of action Metabolism impaired in liver cardiac failure and viral infections ==> higher duration of action
31
Drug interactions of theophylline
Plasma concentration decreased by P450 inducers ( rifampicin, phenytoin, carbamazepine) Plasma concentration increase by p450 inhibitors ( erythromycin , clarithromycin, ciprofloxacin, diltiazem, fluconazole )
32
Muscuranic receptors antagonists
Ipratropium ( main one) Tiotropium (used in maintenance treatment of COPD )
33
Is ipratropium selective
No not selective
34
Ipratropium action
Inhibits mucus secretion in asthma Increase mucociliary clearance No effect on inflammation
35
Maximum effect of muscarinic antagonists
Max effect at 30mins | Persists 3-5h
36
CysLTs antagonists
Montelukast Zafirlukast Pranlukast
37
CystLTs drugs action
Antagonize cysLT1 Reduce active reaction to aspirin Inhibit exercise induced asthma ( early and late response affected ) Relax airways in mild asthma ( less effective than salbutamol) Reduce sputum eosinophilia
38
CystLt mode of administration
Mouth | In combination with corticosteroid
39
Side effect of CYstLTs
Headache | GI Disturbance
40
Anti inflammatory agents
Glucocorticoids Cromiglicate & nedocromil Anti IgE
41
Main drug used for anti inflammation
Glucocorticoid
42
Glucocorticoid
``` Beclometasone Budesonide Fluticasone Mometasone Ciclesonide ```
43
Glucocorticoid mode of administration
Inhalation ( dose metered) | Dry powder
44
Glucocorticoid impact is
Antiinflammatory agent Not bronchodilator Prevent progression of chronic asthma Effective in acute asthma
45
Glucocorticoid mode of action
Decrease formation of cytokines ( mostly th2 cytokines ) Inhibit vasodilator PGE2 and 1 by inhibiting COX 2 Inhibit allergen induced influx of eosinophils into lung Upregulate B2 adrenoreceptor Decreased microvasculature permeability Inhibit production of cytokines Reduced synthesis of IL3 (involved in mast cell production) Yes
46
Some reasons why glucocorticoid therapy does not work sometimes
Less glucocorticoid receptors Reduced activity of histone deacetylase ( in smokers )
47
Unwanted effect of glucocorticoid
Oropharyngeal Candidiasis Sore throat croaky voice Adrenal suppression at regular high dose ( need steroid card )
48
Glucocorticoid not susceptible of causing adrenal supressinn
Fluticasone Mometasone Ciclesonide
49
Cromiglicate and nedicromil action
Weak antiinflammatory effect | Not bronchodilators
50
Cromiglicate and nedicromil mode of administration
Inhalation Aerosols Dry powders Topical for conjuctivitis and rhinitis
51
Why can you give Cromiglicate and nedicromil as prophylactics
Reduce immediate and late asthma responses Reduce bronchial hyper activity
52
Cromiglicate MOA
Mast cell stabilizer Prevent histamine releases Not fully understood and not only action Depress neuronal reflex triggered by stimuli
53
Anti IgE treatment
Omalizumab
54
Omalizumab action
Effective in allergic asthma and allergic rhinitis
55
Why is omalizumab not too much used
Expensive | Still unclear
56
Treatment of status asthmaticus
Oxygen in high conc (more than 60%) Inhalation of nebulized salbutamol IV hydrocortisone Oral prednisolone Sometimes Nebulized ipratropium Iv salbutamol or aminophylline Antibiotics ( of infection)
57
COPD
Chronic inflammatory disease that cause obstruction of airflow from the lungs
58
Main COPD
Emphysema | Chronic bronchitis
59
Presentation of COPD
Morning cough attack Chronic cough with exacerbations Progressive breathlessness
60
Complications of COPD
Pulmonary hypertension Cor pulmonale Respiratory failure
61
Main cause of COPD
Cigarette | Air pollution
62
COPD pathogenesis
Small airway fibrosis Obstruction Destruction of alveoli and elastin fibers in lung parenchyma and Chronic inflammation in small airways and lung parenchyma ( high macrophages, neutrophils , t lymphocytes) Inflammatory mediators not clearly defined as in asthma
63
Treatment of COPD
Stopping smoking Immunization against influenza, pneumococcus because of lethal superimposed infection Glucocorticoids generally ineffective event tho still done because asthma can be superimposed HDAC regulate synthesis of pro inflammatory cytokines. HDAC enhanced by glucocorticoids. When HDAC low , severer COPD HDAC inhibited by smoke so that is why glucocorticoids in COPD does not really work Long acting glucocorticoids eith modest Benefit but does not help with inflammation Chemokines antagonist PDE inhibitors Inhibitors of cell signaling -> p38 mitogen activated Antioxidants Inhibitors of NO synthase Leukotriene B4 antagonist
64
Is there a specific licensed treatment for COPD
No
65
Specific treatment of COPD
Short acting drugs -> ipratropium, salbutamol Long acting drugs -> tiotropium, salmeterol, formoterol Theophylline when CO2 retention Respiratory stimulants like doxapram when acute respiratory failure ( replaced by ventilator support ) Long term oxygen therapy at home when no smoking Broad spectrum antibiotics when infection (cefuroxime) Glucorticoid (iv hydrocortisone , oral prednisolone )
66
How is acute exacerbations treated innCOPD
Inhaled O2 at at least 24% O2

Respiratory Module (5 decks)

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