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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
Q

Side effects of theophylline

A

Act on CNS CVS GI diuresis

Cause insomnia , nervousness etc

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26
Q

What happens when xanthines concentration goes above 200

A

Serious CVS and CNS effects
Dysrhythmias which can be fatal
Seizures (fatal if respiration impaired )

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27
Q

Theophylline mode of administrion

A

Oral sustained release préparation

28
Q

Aminophylline mode of administration

A

Slow IV of loading dose And then IV infusion

29
Q

Theophylline absorbed by

A

GIT

30
Q

Metabolism of theophylline

A

p450 metabolism
Induced by smoking , so less duration of action

Metabolism impaired in liver cardiac failure and viral infections ==> higher duration of action

31
Q

Drug interactions of theophylline

A

Plasma concentration decreased by P450 inducers ( rifampicin, phenytoin, carbamazepine)

Plasma concentration increase by p450 inhibitors ( erythromycin , clarithromycin, ciprofloxacin, diltiazem, fluconazole )

32
Q

Muscuranic receptors antagonists

A

Ipratropium ( main one)

Tiotropium (used in maintenance treatment of COPD )

33
Q

Is ipratropium selective

A

No not selective

34
Q

Ipratropium action

A

Inhibits mucus secretion in asthma

Increase mucociliary clearance

No effect on inflammation

35
Q

Maximum effect of muscarinic antagonists

A

Max effect at 30mins

Persists 3-5h

36
Q

CysLTs antagonists

A

Montelukast
Zafirlukast
Pranlukast

37
Q

CystLTs drugs action

A

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
Q

CystLt mode of administration

A

Mouth

In combination with corticosteroid

39
Q

Side effect of CYstLTs

A

Headache

GI Disturbance

40
Q

Anti inflammatory agents

A

Glucocorticoids
Cromiglicate & nedocromil
Anti IgE

41
Q

Main drug used for anti inflammation

A

Glucocorticoid

42
Q

Glucocorticoid

A 
Beclometasone
Budesonide
Fluticasone
Mometasone
Ciclesonide
43
Q

Glucocorticoid mode of administration

A

Inhalation ( dose metered)

Dry powder

44
Q

Glucocorticoid impact is

A

Antiinflammatory agent
Not bronchodilator
Prevent progression of chronic asthma
Effective in acute asthma

45
Q

Glucocorticoid mode of action

A

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
Q

Some reasons why glucocorticoid therapy does not work sometimes

A

Less glucocorticoid receptors

Reduced activity of histone deacetylase ( in smokers )

47
Q

Unwanted effect of glucocorticoid

A

Oropharyngeal Candidiasis

Sore throat croaky voice

Adrenal suppression at regular high dose ( need steroid card )

48
Q

Glucocorticoid not susceptible of causing adrenal supressinn

A

Fluticasone
Mometasone
Ciclesonide

49
Q

Cromiglicate and nedicromil action

A

Weak antiinflammatory effect

Not bronchodilators

50
Q

Cromiglicate and nedicromil mode of administration

A

Inhalation
Aerosols
Dry powders
Topical for conjuctivitis and rhinitis

51
Q

Why can you give Cromiglicate and nedicromil as prophylactics

A

Reduce immediate and late asthma responses

Reduce bronchial hyper activity

52
Q

Cromiglicate MOA

A

Mast cell stabilizer
Prevent histamine releases
Not fully understood and not only action

Depress neuronal reflex triggered by stimuli

53
Q

Anti IgE treatment

A

Omalizumab

54
Q

Omalizumab action

A

Effective in allergic asthma and allergic rhinitis

55
Q

Why is omalizumab not too much used

A

Expensive

Still unclear

56
Q

Treatment of status asthmaticus

A

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
Q

COPD

A

Chronic inflammatory disease that cause obstruction of airflow from the lungs

58
Q

Main COPD

A

Emphysema

Chronic bronchitis

59
Q

Presentation of COPD

A

Morning cough attack
Chronic cough with exacerbations
Progressive breathlessness

60
Q

Complications of COPD

A

Pulmonary hypertension
Cor pulmonale
Respiratory failure

61
Q

Main cause of COPD

A

Cigarette

Air pollution

62
Q

COPD pathogenesis

A

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
Q

Treatment of COPD

A

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
Q

Is there a specific licensed treatment for COPD

A

No

65
Q

Specific treatment of COPD

A

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
Q

How is acute exacerbations treated innCOPD

A

Inhaled O2 at at least 24% O2

Respiratory Module (5 decks)

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