COPD Flashcards

1
Q

** disorder **: Destruction of alveoli and elastin fibres in the lung. May be caused by proteases released during the inflammatory response. Causes respiratory failure. Destruction of alveoli impairs gas transfer

A

Empyhsema

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2
Q

** Disorder **
* Attacks of winter morning cough
* Progresses to chronic cough with intermittent exacerbations
* Often initiated by an upper respiratory
infection

A

Bronchitis

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3
Q

main aim in COPD treatment

A

to reduce the progression of the disease, however does not supress inflammation or prevent the development of Emphysema

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4
Q

1st step in management of COPD

A

1) Smoking cessation –>Slows the progress of COPD
2) Immunizations –> Superimposed infections are potentially lethal

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5
Q

Drugs used in the treatment of COPD

A

1) Bronchodilators - β2 Adrenoreceptor agonists
2) Muscarininc receptor anatgonsits
3) Corticosetroids (CS)

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6
Q

short-acting drugs used in the tx of COPD

A

Short-acting drugs
1) Short-acting anti-muscarinic antagonists (SAMA):
Ipratropium

2) Short-acting beta agonists (SABA): salbutamol

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7
Q

Long-acting drugs used in the tx of COPD

A

Long-acting drugs
1) Long-acting anti-muscarinic antagonists (LAMA) :
Tiotropium

2) Long-acting beta agonists (LABA): salmeterol or
formoterol
(LABA)

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8
Q

Muscarinic receptor antagonists used in the tx of COPD?

A

1) Ipratropium (Short-Acting Muscarinic Antagonist-SAMA)
2) Tiotropium (Long-Acting Muscarinic Antagonist-LAMA)

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9
Q

Adm of Ipratropim

A
  • Inhalational
  • Maximum effect: approximately 30 min after inhalation
  • Persists for 3–5 h
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10
Q

Max effect of Ipratropium starts approx. —– after inhalation

A

30 min

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11
Q

Duration of Action of Ipratropium

A

3-5 hrs

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12
Q

Adm of Tiotropium

A

Inhalation

 Longer-acting (t1/2=35 hours)
 More potent than ipratropium

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13
Q

Which is more potent Ipratropium or Tiotropium?

A

Tiotropium

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14
Q

Duration of action of Tiotropium

A

Longer-acting (t1/2=35 hours)

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15
Q

AE of Muscarinic receptor agonists

* Ipratropium, Tiotropium

A

1) Dry mouth
2) Dry eyes
3) Raised intraocular pressure and blurred vision
(Caution in glaucoma)
4) Metallic taste
5) Constipation
6) Tachycardia (Caution in CV disease)
7) Urinary retention (Caution)
8) Cough/hoarse voice

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16
Q

Contraindications of Muscarinic receptor agonists

A

1) Glaucoma (raised intraocular pressure and blurred vission)
2) CV disease (Tachycardia)
3) Urinary retention

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17
Q

CU of Tiotropium

A

1) LAMA added w/ LABA when control insufficient
2) COPD

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18
Q

CU of Ipratropium

A

1) In Acute sever asthma, SAMA added w/ SABA which aguments (increases) bronchodilation of SABA
2) COPD

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19
Q

treatment approach to reduce inflammation in COPD

A

ICS (inhaled corticosteroids)

  • note: oral corticosteroids should not be given to patients with stable COPD
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20
Q

MoA of inhaled corticosteroids in the management of COPD

A

1) Aim is to temper inflammation about COPD (tx not monotherpay)
2) Decrease frequency of exacerbation and improve quality of life

* not as effective in asthma

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21
Q

CU of Theophylline in COPD

A

tx of asthma and COPD esp in patients who tend to reatins CO2

  not recommended due to its uncertain benefits!!!
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22
Q

What can you to give patients w/ sever COPD and Hypoxaemia?

A

Long-term O2 therapy (Adm at home)

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23
Q

Tx approach for Acute COPD exacerbation

A

1) Inhaled O2
2) Broad-spectrum abx if there is evidence of infection
3) Inhaled bronchodilators for symptomatic
improvement (SABA)
4) Oral prednisolone (CS)

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24
Q

Anti-Histamine 1st generation examples

A

diphenhydramine,
promethazine,
chlorpheniramine,
meclizine,
dimenhydrinate,
hydroxyzine

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25
MoA of 1st gen Anti-Histamins
Reversible competitive antagonists of H1 receptors **(cross BBB)**
26
AE of Anti-Histamine
1) **Sedation** caused by CNS histamine receptor blockage 2) **Blurred vission, Dry mouth, Urinary retention** --> Muscarinic receptor blockade 3) **Headache** -> α1-Adrenergic receptor blockade
27
MoA of Hitamine-1 Recptors
1) Bronchoconstriction 2) Increased vascular permeability 3) Itching 4) Nasal irritation/sneezing/ congestion 5) Vasodilation
28
CU of 1st gen Anti-Histamins
1) Allergic reactions, rhinitis, urticaria 2) Cold medication (tx of symptoms) 3) Sleep aid 4) **Pre-op sedation** 5) Nausea/vomiting 6) Motion sickness, vertigo
29
2nd gen Anti-histamines
Loratadine Desloratadine Fexofenadine Cetirizine -adine
30
CU of 2nd gen Anti-Histamines
allergy
31
why are 2nd gen Anti-Histamines preferred over 1st gen?
Because they are less sedative as they have decreased penetrance into CNS
32
AE of 2nd gen Anti-Histamines
Uncommon
33
main aim in the treatment of Cough supression
Best to treat underlying cause rather than cough
34
drugs used to supress cough
**weak Opoids** Codeine Pholcodeine Morphine
35
CU of Morphine in respiratory disease
Palliative (soothing) care in **lung cancer cough**
36
which opoids are the most to least addictive **Codeine, Morphine, Pholcodeine**
least --> most **Phlocodeine < Codeine < Morphine**
37
AE of Opiods
1) Constipation 2) Drowsiness 3) Dry mouth 4) **Miosis ("pin point pupil")** 5) Nausea/vomiting 6) **Respiratory depression**
38
Opiods are avoided in?
**chronic pulmonary infection and asthma** why? * Thickening of mucus and retention * Risk of **respiratory depression**
39
Morphine Derivative
Dextromethorphan
40
AE of Dextromethorphan
Uncommon; dizziness, nausea, vomiting, or GI disturbance
41
MoA of Dextromethrophan
* **Binds σ receptors** * Also binds serotonergic receptors -> **inhibits reuptake of serotonin**
42
Contraindications of Dextromethorphan
**serotonergic agents** --> may cause **Seratonin syndrome**
43
Dextromethorphan at high doses can antagonize **--------** receptors
**Glutamate NMDA**
44
class of N-acetyl cysteine
Mucolytic
45
CU of N-acetyl cysteine
1) Antidote for patracetamol 2) Cystic Fibrosis
46
MoA of N-acetyl cysteine (as a mucolytic)
1) Depolymerizes the mucin glycoprotein oligomers via disulfide bond hydrolysis 2) **Decreases mucus viscosity**
47
AE of N-acetyl cysteine
nausea, vomiting, flushing, rash
48
peptide Mucolytic
Dornase alfa
49
MoA of Dornase alfa
depolymerizes DNA
50
CU of Dornase alfa
Cystic fibrosis
51
class of Hypertonic Saline
Mucolytic
52
# * i dont think its important MoA of Hypertonic saline
* Disrupts ionic bonds within the mucus gel * Dissociates DNA from mucoproteins allowing natural proteolytic enzymes to digest the mucoprotein
53
**------**: a type of cough medicine used to help clear mucus (phlegm) from your airway
Experctorant
54
Experctorant example
**Guaifenesin**
55
CU of Guaifenesin
symptomatic relief of acute **productive cough**
56
MoA of Guanifenesin
* Increases the volume of respiratory secretions * Decreases the viscosity of bronchial secretions * Does not suppress the cough reflex
57
How are Guaifenesin used?
Used alone or in combination with antihistamines, cough suppressants, and decongestants
58
Decongestants examples
Pseudoephedrine Phenylephrine
59
Moa of Phenylephrine
**Selective α1 adrenergic agonist** (Less CNS stimulation than pseudoephedrine)
60
ΜοΑ of Pseudoephedrine
α1 adrenergic agonist -> release of norepinephrine
61
ΑΕ of Pseudoephedrine
**CNS stimulation**, anxiety, hypertension, urinary retention, tachycardia, nausea/vomiting
62
Pseudoephedrine is a **--------** precursor
Methamphetamine