Pharmacology > Respiratory system > Flashcards

Respiratory system Flashcards

(46 cards)

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1
Q

Respiratory is controlled in the….

A

Medulla

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2
Q

Autonomic nervous system

A

-controls rate and depth through smooth muscle contraction/relaxation

Sympathetic - noepinephrine –> bronchodilation - B2 adrenergic receptors
Parasympathtic - acethycholine - bronchoconstriction - M3 cholinergic receptors

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3
Q

Mucosal edema, secretions, bronchospasms - they…

A

increase the resistance to airflow; decrease ventilation and diffusion of gases

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4
Q

Parasympathetic system

A
  • innervation –> smooth muscle and secretory glands

- causes broncho-constriction by activation of muscarinic receptors; increase mucous production

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5
Q

Treatment of COPD

-effectiveness of non-selective anti-muscarinic drug

A
  • not very useful
  • inhibit M2 and M3 –> acetylcholine is released –> block on M3 will not be that effective –> competition between blocking agent and acetycholine –> can oppose bronchodilation

-used before the administration of inhalant anesthetics to reduce the accumulation of secretions in the trachea and the possibility of laryngospasms

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6
Q

Sympathetic system

A

-beta-2-adrenoreceptors in bronchial smooth muscle

short acting beta-2-agonists: acute treatment of asthma symptoms
long acting beta-2-agonists: chronic asthma treatment should only be used in combination with steroids, also COPD

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7
Q

Mechanism of response to inhaled irritants

A

Provoke bronchoconstriction by:

  1. trigger the release of chemical mediators from mast cells
  2. stimulate afferent receptors to initiate reflex bronchoconstriction or to release tachykinins that directly stimulate smooth muscle contraction
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8
Q

Respiratory system - man issues: (4)

A
  1. Bronchospasm
  2. Mucus secretion
  3. Cough
  4. Inflammation
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9
Q

Drugs that cause

  1. Bronchodilation
  2. Bronchoconstriction
A
  1. beta agonists –> increase cAMP

2. Muscarinic antagonists

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10
Q

Asthma (5)

A
  • acute and chronic
  • irritants: cold, dry air, exercise-induced, thermally induced
  • attacks may be triggered by inflammatory response and/or bronchospasms
  • early and late reaction - different mediators in each of them
  • treatment: bronchodilators –> increase cAMP
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11
Q

Asthma

-early reaction (5)

A
  • FEV decrease
  • allergen bind to mast cell –> degranulation
  • bronchoconstriction
  • activation of many inflammatory cells - mast cells, T lymphocyte
  • different mediators are released - Histamine, IL-4,5, TNF, TGF
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12
Q

Asthma

-late reaction (3)

A
  • edema, mucous hyperesecretion, smooth muscle contraction, increase bronchial reactivity
  • cytokines are release which will also activate different inflammatory cells
  • cells –> eosinophil, neutrophil
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13
Q

B2-adrenoreceptor agonists

  • names
  • mechanism of action
A

-Salbutamol, Salmeterol, Formoterol

  • causes bronchodilation –> relieving bronchospasms
  • decrease mediator release from mast cells and TNF-a release from monocytes –> increase mucus clearance by an action on cilia
  • effect on the early phase
  • increase severity of the late reaction –> should be used with inhaled corticosteroids
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14
Q

B2-adrenoreceptor agonists

  • unwanted effects
  • Short acting beta-2 agonists
  • Long acting beta-2 agonists
A
  • tachycardia - if it reaches systemic circulation
  • Salbutamol - fast onset and short duration
  • Salmeterol - slow onset and long duration
  • Formoterol - fast onset and long duration
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15
Q

Other adrenoreceptor agonists

  • names
  • why are they not used?
A

-Ephedrine, Adrenaline (epinephrine)

  • less suitable, less safe because they could cause arrhythmias and other side effects
  • used for emergency treatment
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16
Q

Xanthine derivatives

  • name
  • pharmacokinetics (6)
A

-Aminophylline

  • well absorbed in the GI tract
  • sustained-release tablet
  • many drug-drug interactions - plasma clearance varies
  • metabolized in the liver
  • clearance decrease in viral infections
  • narrow therapeutic window
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17
Q

Xanthine derivatives - Aminophylline

  • indications
  • unwanted effects
A

-acute and chronic asthma, COPD

  • tremulousness, nausea, vomiting, arrhythmias (increase heart rate)
  • those effect due to cAMP levels increasing, increase GCMP, adenosine antagonism
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18
Q

Xanthine derivatives

-mechanism of action

A
  1. inhibit PDE3 = relaxing smooth muscles –> increase intracellular cAMP
  2. inhibit PDE4 = decrease release of cytokines and chemokines
  3. inhibit cell surface receptors for adenosine (adenosine provokes contraction of smooth muscle and histamine release)
  4. low-dose enhance the effectiveness of corticosteroid treatment
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19
Q

Anti-muscarinic bronchodilators

  • names
  • mechanism of action
Study These Flashcards
A

-Ipratropium, Tiotropium

  • block the contraction of airway smooth muscle caused by vagus nerve and the secretion of mucus
  • block acethycholine –> decrease IP3 –> decrease calcium
  • inhibit only that portion of the response mediated by muscarinic receptors, which varies by stimulus
20
Q

Anti-muscarinic bronchodilators

  • effect on which phase?
  • indications
  • unwanted effects
Study These Flashcards
A
  • NO EFFECT ON EARLY AND LATE INFLAMMATION PHASES
  • COPD - long acting, asthma, bronchospasms precipitaded by beta-2-agonists
  • dry mouth
21
Q

Ipratropium

-indication

Study These Flashcards
A

bronchopasms caysed by bronchitis, asthma, beta 2 agonists, COPD

slow onset of action
short duration of action

22
Q

Tiotropium

-indication

Study These Flashcards
A

COPD

slow onset of action
long duration of action

23
Q

Corticosteroids

  • names
  • mechanism of action
Study These Flashcards
A

-Budesonide, Fluticasone

  • anti-inflammatory effect –> inhibit the production of inflammatory cytokines
  • inhibit the infiltration of airways by lymphocytes, eosinophils, mast cells
  • reduce bronchial hyper-reactivity and reduce the frequency of asthma exacerbations
  • potentiate the effect of beta receptor agonists - bronchodilation
  • effect in EARLY AND LATE RESPONSE
24
Q

Corticosteroids

  • indication
  • unwanted effects
Study These Flashcards
A
  • improve all indices of asthma control
  • chronic asthma
  • acute asthma
  • inhaled forms are gold strandard
  • oral forms are used only in late stages of the disease - too many side effects
  • no general adverse effects
  • local effects of inhaled forms: candidiasis of the mouth or throat, hoarseness
25
Cromoglycates - names - mechanism of action
-Cromoglicate - causes hyperpolarization of the cells --> decrease their activity - inhibit mast cells and eosinophils activation - inhibit antigen and exercise induce asthma --> prevents bronchoconstriction - decrease airway reactivity, decrease symptomatic severity - inhibit cough - no effect on airway smooth muscle tone, ineffective in reversing bronchospasm
26
Cromoglycates - pharmacokinetics - indications - unwanted effects
- inhaled - not very potent - inhibit EARLY AND LATE RESPONSES -prophylaxis of acute asthma attacks - toxicity minimal - transient bronchospasm - beta-2-agonist may be inhaled a few minutes before
27
Leukotriene pathway inhibitors | -names
- Leukotriene receptor antagonist – Montelukast - 5-Lipoxygenase inhibitor – Zileuton - inhibit leukotriene type 1 receptor - inhibit EARLY AND LATE RESPONSES - decrease sputum eosinophils - bronchodilation in mild asthma
28
Why shouldn't aspirin be used in patients with asthma?
1. Aspirin inhibits COX irreversibly 2. Shifts arachidonic acid towards another pathway 3. LOX levels increase 4. Leukotrienes levels increase Leukotrienes could cause bronchoconstriction, mucous secretion, macrovascular leakage, coudl facilitate chemotaxis
29
Leukotriene pathway inhibitors - indications - unwanted effects
- exercise-induced asthma - aspirin-induced asthma - Montelukast - Churg-Strauss syndrome (systemic vasculitis, worsening asthma) - Zileuton - liver toxicity
30
Anti-IgE Monoclonal Antibodies - names - mechanism of action
-Omalizumab - decrease the frequency and severity of asthma exacerbations - inhibits binding of IgE --> does not provoke mast cell degranulation - inhibit EARLY AND LATE RESPONSES
31
Anti-IgE Monoclonal Antibodies - indications - unwanted effects
-patients 12 years or older with moderate-to-severe allergic asthma - anaphylaxis - Churg-Strauss syndrome
32
Treatment steps of asthma
1. short acting beta agonists 2. + preventing therapy - inhaled corticosteroid 3. long acting beta agonists + dose of inhaled corticosteroid may also be increased 4. high dose inhaled corticosteroids 5. regular oral corticosteroid
33
Acute asthma attack | -drugs that can be used (5)
1. Salbutamol - short acting beta agonists 2. Epinephrine - systemic beta agonist 3. Aminophylline 4. Ipratropium - short acting anti-muscarinic agent 5. Corticosteroids
34
Asthma vs. COPD
ASTHMA - largely reversible airflow limitation - corticosteroids are effective - normally parenchyma is not involved, damage to epithelium - no abundant mucous secretion - key cells: eosinophilic inflammation - large airways - all airways are involved - thickened b.m due to substances released from eosinophils during the late phase - therapy- goal --> control symptoms and maintain close to normal pulmonary function, exacerbation can be prevented COPD - largely irreversible airflow limitation - limited effect with corticosteroids - heavy mucous secretion - key cells: neutrophilic inflammation - small airways - damage is caused in the peripheral part --> alveoli - late stages --> hard to normalize airflow - usually in older people - metaplasia - high risk factor for pulmonary cancer - defective response of inflammatory cells - therapy- goal --> relief symptoms, prevent complications and improve life style
35
COPD (4)
- limitation of airflow that is not reversible --> progressive - caused by a mixture of small airway disease and parenchymal destruction - abnormal inflammatory response of lung to harmful substances - treatment: no medications can alter the course of the disease. goal is to relief symptoms, prevent complications and improve life style
36
COPD | -treatment (2)
- Bronchodilators: inhaled therapy is preferred, long- acting ones are more effective - beta agonists, anti-muscarinic, theophylline - Corticosteroids - not very effective - long term treatment is not recommended - more effective when combined with a long-acting beta agonist
37
Inhalation devices
-increase delivery of drug to the lungs and decrease deposition of drug on the oropharyngeal mucosa
38
Anti-tussives - central acting - names - mechanism of action - indications - adverse effects - warning
- Codeine - block central parts of the cough reflex - dry, hacking, non-productive cough - respiratory depression - excessive suppression of the cough reflex
39
Anti-tussives - peripheral acting - names - mechanism of action - indications - adverse effects - contraindications
-Prenoxdiazine - blocks peripheral parts of the cough reflex - local anesthetic and broncholytic actibity - relief dry cough - allergic reactions, dry mouth - hypersensitivity to the drug, high bronchial secretions
40
Expectorants - names - mechanism of action
-Guaifenesin - stimulate the flow of respiratory tract secretions - increases the efficiency of the cough reflex and facilitate removal of the secretions - increase the volume and decrease the viscosity of the secretion in the trachea and bronchi - allow ciliary movement - muscle relaxant and anti-convulsant properties
41
Expectorants - adverse effects - drug interactions
- nausea, vomiting, diarrhea, kidney stones, allergic reactions, dry mouth, constipation - paracetamol, aspirin, alcohol, sleep-pills
42
Mucolytics | -names
Acetylcysteine | Dornase Alfa
43
Mucolytics - Acetylcysteine - mechanism of action - indications - unwanted effects
- rapidly metabolized to cysteine - decrease disulphide bonds --> reduce viscosity and elasticity of the mucus - decrease several inflammatory mediators - interact directly with oxidants - paracetamol overdose, mucolytic, COPD, cystic fibrosis - nausea, vomiting, allergic reactions, fever
44
Mucolytics - Dornase alfa - mechanism of action - indications - unwanted effects
- enzyme selectively cleaves DNA (non cellular) - hydrolyzes the DNA present in sputum/mucus and reduces viscosity - cystic fibrosis - voice disorders, laryingitis, transient skin rash
45
Nasal decongestants - name - mechanism of action
-Pseudoephedrine, Xylometazoline - used directly - for short-term basis: no more than 7 days --> could cause tissue necrosis - alpha-1-adrenoreceptors agonists - constrict blood vessels in respiratory tract
46
Nasal decongestants - indications - side effects - contraindications
- nasal congestion - allergic rhinitis - hypotension - shock - irritation of the nose - closed angle glaucoma
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