Wheeze/Stridor Pharm Flashcards

1
Q

What is the GOLD treatment recommendation for COPD

A

Self-manage education and smoking cessastion

Bronchodialators

Inhaled corticosteroids

Pulm rehab, oxygen, surgery pretty low on list

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2
Q

REcommended meds for low risk, less symptomatic COPD

A

Short acting anticholinergic or short acting B2-agonist

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3
Q

Tx option for Low risk, more symptoms COPD

A

Long acting anticholinergic, Long acting B2 agonist

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4
Q

Tx option for higher risk, less symtpoms COPD

A

Inhaled corticosteroid + long acting B2agonist

OR
Long acting anticholinergic

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5
Q

Tx for High risk, symptomatic COPD

A

Inhaled corticosteroid + long act B2 agonist

OR

Long acting anticholinergic

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6
Q

What is albuterol?

What about Ipratropium bromide?

A

albuterol = SABA

Ipratropium Bromide = short acting anticholinergic antagonist

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7
Q

What are two Long acting beta2 adrenergic agonist (LABA)

A

Sotolol and Formoterol

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8
Q

What type of drug is tiotropium

A

Long acting anticholinergic antagonist

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9
Q

Beclomethasone, Fluticasone and Budesonide are all:

A

Inhaled corticosteroids

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10
Q

What meds are recommended to manage acute exacerbations of COPD?

A

bronchodialators: SABA (Albuterol), Short acting anticholingergic agonists (ipratropium bromide)

Systemic corticosteroids (oral prednisone)

Antibiotics or O2 therapy

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11
Q

What is the mechanism of theophyline

A

inhibits PDE so we can increase levels of cAMP which promotes Bronchodialation

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12
Q

What effects does theophyline have throughout the body?

A

Decreases: eosinophils, mast cells, macrophages

cause bronchodialation, and decrease leaky vessels

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13
Q

what can happen with high conc of theophyline?

A

At high concentrations, cardiac arrhythmias may occur as a consequence of inhibition of cardiac PDE3 inhibition and antagonism of cardiac A1 receptors.

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14
Q

Where do the majority of inhaled corticosteroids go?

A

60-90% lands in mouth and is swallowed–> to GI adn metabolized by liver with 10-40% getting to lungs

thus get systemic side effects from use

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15
Q

What happens to the HPA axis with prolonged corticosteroid use?

A
  • Corticosteroids inhibit ACTH and cortisol secretion by a negative feedback effect on the pituitary gland
  • Hypothalamic-pituitary-adrenal (HPA) axis suppression depends on dose
  • Significant suppression after short courses of corticosteroid therapy is not usually a problem, but prolonged suppression may occur after several months or years.
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16
Q

What are side effects of long term oral corticosteroid use?

A
  • fluid retention
  • increased appetite
  • weight gain
  • osteoporosis
  • capillary fragility
  • hypertension
  • peptic ulceration
  • diabetes
  • cataracts
  • psychosis.
  • frequency tends to increase withage.
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17
Q

What is steroid withdrawl syndrome?

A

after long use, need to get off them slowly: see lethargy, musckuloskeletal pains, fever, HPA suppresion see when use more then 2000mg a day

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18
Q

What are systemic side effects seen with inhaled corticosteroids?

A

dermal thinning, cataracts, osteoporosis, concern with growth in children

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19
Q

What are local side effecs seen from inhaled steroids?

A
  • Dysphonia (hoarse voice)
  • Topical candidiasis (thrush)
  • Contact hypersensitivity
  • coug
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20
Q

What is the most likely reason that inhaled anticholinergic drugs are effective in COPD?

A

Block vagally mediated airway tone

21
Q

• Anticholinergic drugs may be as effective as or even superior to____

drugs inhibit vagally mediated airway tone, thereby producing _____

A

β2 agonists.

22
Q

Role of vagal tone in the airways

A

causes release of Ach to control tone in bronchioles, but in pt with COPD, they become highly constricted thus vagal tone decreases airway = bad

use a muscarininc antagonist to counteract this

23
Q

What are COPD pts more sensitve to vagal input to the bronchi?

A

This effect is small in normal airways but is greater in airways of patients COPD

 which are structurally narrowed and have higher resistance to airflow because airway resistance is inversely related to the fourth power of the radius (r).

24
Q

reduce air trapping and improve exercise tolerance in COPD patients.

A

Anticholinergic drugs

25
Q

What is a common anticholinergic drug used for COPD pts?

A

Ipratropium bromide

26
Q

What are some neg sides of ipratropium bromide?

A

• Dry mouth

  • Constipation
  • blurred vision
  • dyspepsia
  • cognitive impairment
27
Q

The chronic use of albuterol in treatment of COPD (or asthma) is associated with the development of

A

tolerance

28
Q

Define tolerance

A
  • attenuated response to the repeated use of the drug
  • may be due to down-regulation of the receptor
29
Q

What are some adverse effects of B2 selective agonists

A

tremor, tachycardia, hypokalemia, restlessness, hypoxemia

dose related: d/t excessive activation of extrapulmonary B receptors

30
Q

What type of pts should be careful when useing B2 selective agnostis to manage COPD

A

those with CV disease more at risk for adverse reactions

31
Q

What is the benefit of combination therapy with a steroid and LABA?

A
  • steroids increase the transcription of the β2 receptor gene, prevent down-regulation of β2 receptors, increase β adrenergic responsiveness, reverse β receptor desensitization in airways
  • β2 Agonists enhance the action of GR(glucocorticod receptor corticosteroids bind), increased nuclear translocation of liganded GR receptors, enhancing the binding of GR to DNA.
  • β2 agonists and corticosteroids enhance each other’s beneficial effects in asthma therapy.
32
Q

What are the thearpeutic management goals of asthma?

A

No symptoms (day or night)

No exacerbations (serious attacks or flare-ups)

Normal physical activity

Normal or near-normal lung function

Minimal use of rescue medicine

33
Q

What is the preferred PRN for asthma?

A

SABA

34
Q

What is the preferred management for person with asthma that needs more help then just prn?

A

low dose inhaled glucocorticoid + LABA

OR

medium dose inhaled glucocorticoid

35
Q

Albuterol is used as what for asthma?

A

reliever: SABA

36
Q

controller medication for asthma that is a inhaled corticosteroid

A

Beclomethasone

37
Q

controller medication for asthma that is a Leukotrine receptor antagonist

A
  • Zafirlukast
  • montelukast
38
Q

What is the MOA of Zileuton

A

Leukotriene synthesis inhibitor

39
Q

What is the MOA of Omalizumab

A

Anti-IgE therapy: binds to free IgE so it cant bind to mast cells (thus IgE cant crosslink when exposed to their allergen)

40
Q

What is the pathophysiological basis for why bronchodilators are not the sole agent in the treatment of asthma?

A

because there is an immediate early reaction that deals with bronchocnx followed by transient recover ,

but we have a delayed reponse that is Hyperresponsive and inflammatory so we need to adress that as well

41
Q

Your patient is a 62-year old female with hypertension and asthma. Which antihypertensive drug should be avoided in this patient?

A

Propranolol: B1 and B2 adrengeric antagonist while albuterol is a B2 adrenergic Agonist

need to use B1 selective antagonist: metoprolol

42
Q

What is (are) a major limitation(s) to the use of omalizumab in treatment of asthma?

A

It’s too expensive

It only treats allergic forms of asthma

It is has to be given by injection

Takes 12 weeks of treatment to see effects

Anaphylaxis

43
Q

What is the key pathology of COPD

A

Mucous gland metaplasia, loss of alveolar tissue

Inflammation: Macorphages and Neutrophils ++

this is CD8+ mediated

44
Q

Key pathology of asthma

A

Mucous gland hyperplasia, intact alveolar structures

Mast cells and eosinophils++

CD4+

45
Q

Test results for COPD

Spriometry:

Diffusing capacity:

Chest xray:

A

Spriometry: obstruction not fully reversible

Diffusing capacity: reduced

Chest xray: Hyperinflation, bullous changes

46
Q

Test results for ASthma

Spriometry:

Diffusing capacity:

Chest xray:

A

Spriometry: obstruction fully reversible

Diffusing capacity: normal or increased

Chest xray: Hyperinflation or normal

47
Q

What treats the primary symptoms of bronchoconstriction in asthma and COPD?

A

Bronchodilators:

Beta2 adrenergic agonists, anticholinergics, theophylline

48
Q

What reduces the level of airway smooth muscle hyperresponsiveness resulting from airway inflammation?

A

“control medication” and its more used in asthma then COPD

49
Q

Whats something we can use to tx acute exacerbations of COPD?

A

antibiotics