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Systemic Pharma- Respiratory + Endocrine > COPD > Flashcards

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
Q

MoA of 1st gen Anti-Histamins

A

Reversible competitive antagonists of H1
receptors
(cross BBB)

26
Q

AE of Anti-Histamine

A

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
Q

MoA of Hitamine-1 Recptors

A

1) Bronchoconstriction
2) Increased vascular permeability
3) Itching
4) Nasal irritation/sneezing/ congestion
5) Vasodilation

28
Q

CU of 1st gen Anti-Histamins

A

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
Q

2nd gen Anti-histamines

A

Loratadine
Desloratadine
Fexofenadine
Cetirizine

-adine

30
Q

CU of 2nd gen Anti-Histamines

A

allergy

31
Q

why are 2nd gen Anti-Histamines preferred over 1st gen?

A

Because they are less sedative as they have decreased penetrance into CNS

32
Q

AE of 2nd gen Anti-Histamines

A

Uncommon

33
Q

main aim in the treatment of Cough supression

A

Best to treat underlying cause rather than cough

34
Q

drugs used to supress cough

A

weak Opoids
Codeine
Pholcodeine
Morphine

35
Q

CU of Morphine in respiratory disease

A

Palliative (soothing) care in lung cancer cough

36
Q

which opoids are the most to least addictive
Codeine, Morphine, Pholcodeine

A

least –> most
Phlocodeine < Codeine < Morphine

37
Q

AE of Opiods

A

1) Constipation
2) Drowsiness
3) Dry mouth
4) Miosis (“pin point pupil”)
5) Nausea/vomiting
6) Respiratory depression

38
Q

Opiods are avoided in?

A

chronic pulmonary infection and asthma

why?
* Thickening of mucus and retention
* Risk of respiratory depression

39
Q

Morphine Derivative

A

Dextromethorphan

40
Q

AE of Dextromethorphan

A

Uncommon; dizziness, nausea, vomiting,
or GI disturbance

41
Q

MoA of Dextromethrophan

A
  • Binds σ receptors
  • Also binds serotonergic receptors -> inhibits reuptake of serotonin
42
Q

Contraindications of Dextromethorphan

A

serotonergic agents –> may cause Seratonin syndrome

43
Q

Dextromethorphan at high doses can antagonize ——– receptors

A

Glutamate NMDA

44
Q

class of N-acetyl cysteine

A

Mucolytic

45
Q

CU of N-acetyl cysteine

A

1) Antidote for patracetamol
2) Cystic Fibrosis

46
Q

MoA of N-acetyl cysteine (as a mucolytic)

A

1) Depolymerizes the mucin glycoprotein oligomers
via disulfide bond hydrolysis
2) Decreases mucus viscosity

47
Q

AE of N-acetyl cysteine

A

nausea, vomiting, flushing,
rash

48
Q

peptide Mucolytic

A

Dornase alfa

49
Q

MoA of Dornase alfa

A

depolymerizes DNA

50
Q

CU of Dornase alfa

A

Cystic fibrosis

51
Q

class of Hypertonic Saline

A

Mucolytic

52
Q

* i dont think its important

MoA of Hypertonic saline

A
  • Disrupts ionic bonds within the mucus gel
  • Dissociates DNA from mucoproteins allowing natural
    proteolytic enzymes to digest the mucoprotein
53
Q

——: a type of cough medicine used to help clear mucus (phlegm) from your airway

A

Experctorant

54
Q

Experctorant example

A

Guaifenesin

55
Q

CU of Guaifenesin

A

symptomatic relief of acute
productive cough

56
Q

MoA of Guanifenesin

A
  • Increases the volume of respiratory secretions
  • Decreases the viscosity of bronchial secretions
  • Does not suppress the cough reflex
57
Q

How are Guaifenesin used?

A

Used alone or in combination with antihistamines,
cough suppressants, and decongestants

58
Q

Decongestants examples

A

Pseudoephedrine
Phenylephrine

59
Q

Moa of Phenylephrine

A

Selective α1 adrenergic agonist
(Less CNS stimulation than pseudoephedrine)

60
Q

ΜοΑ of Pseudoephedrine

A

α1 adrenergic agonist -> release of norepinephrine

61
Q

ΑΕ of Pseudoephedrine

A

CNS stimulation, anxiety, hypertension, urinary retention, tachycardia, nausea/vomiting

62
Q

Pseudoephedrine is a ——– precursor

A

Methamphetamine

Systemic Pharma- Respiratory + Endocrine (6 decks)

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