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hlsc final > Asthma > Flashcards

Asthma Flashcards

1
Q

Asthma

A

Sense of breathlessness and tightness of chest

wheezing, dyspnea, cough

cause: immune-related airway inflammation

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2
Q

events leading to inflammation and bronchoconstriction

A

1) Allergen molecule binds to IgE on mast cells

2) Mast cells release mediatotors
–> bronchocontrictions
–> infiltration of inflammatory cells

3) inflammatory cells release more mediators

RESULT: airway inflammation characterized by edema, mucus plugging, smooth muscle hypertrophy = airflow obstruction

4) inflammation cause by bronchial hyperactivity

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3
Q

COPD symptoms result from 2 processes

A

1) Chronic bronchitis
- cough, excessive sputum
- hypertrophy of mucus-secreting glands in epithelium of large airways

2) Emphysema
- enlarged airspace within bronchioles and alveoli
- deterioration of walls of air spaces

Both caused by rxn to cigarette smoke

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4
Q

Major Drugs for Asthma and COPD: 2 classes

A

1) Antiinflammatory agents
Glucocorticoids: admin on fixed schedule

2) Bronchodilators
B2 aagonist: fixed schedule or as needed
- inhaled

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5
Q

Benefits of inhalation

A

direct to site of action

systemic effects minimized

rapid relief of acute attacks

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6
Q

Glucocorticoid drugs

A

Beclomethasone (inhaled)

Prednisone (PO prototype)

  • most effective for long term control of airway inflammation
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7
Q

Beclomethasone (inhaled)

Prednisone (PO prototype)

Mechanism

A

decrease synthesis and release of inflammatory mediators (leukotrienes, histamines, prostaglandins)

Decreased infiltration and activity of inflammatory cells (eosinophils, leukocytes)

Decreased edema of airway mucosa

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8
Q

Beclomethasone (inhaled)

Prednisone (PO prototype)

Therapeutic use

A

control inflammation in both asthma and COPD

effective for asthma prophylaxis and management of COPD exacerbations

don’t alter course of conditions
- provide management of symptoms

inhalation use: very effective, fist line therapy

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9
Q

Prednisone (PO prototype) use

A

when symptoms cant be controlled with inhaled meds

moderate to severe asthma

high potential for toxicity
- treat brief as possible

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10
Q

Beclomethasone (inhaled)

Adverse effects

A

inhaled - devoid of serious toxicity

  • high doses: oropharyngeal candidiasis (thrush), dysphonia (speaking difficulty)
  • long-term high dose: adrenal suppression ( adrenal glands don’t make enough cortisol)
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11
Q

Prednisone (PO prototype) adverse effects

A

prolonged therapy: adreanal suppression, osteoporosis, immunosuppression

KEY: transferring from PO to inhaled requires several months for recovery of adrenocortical function

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12
Q

Beclomethasone (inhaled)

preparations

A

regular schedule

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13
Q

Prednisone (PO prototype) prepations dose and administration

A

methylprednisone, prednisone are preferred

adult dose 40-60 mg/day for 3-10 days
children: lower

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14
Q

Leukotriene receptor antagonists (LTRAs)

A

suppress leukotriene
- leukotriene involved in recruitment of eosinophils and other inflammatory cells

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15
Q

Types of LTRAs

A

Zileuton
- blocks leukotriene synthesis

Montelukast
- block leukotriene receptor

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16
Q

Leukotrienes

A

promote smooth muscle contraction, vessel permeability and inflammation

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17
Q

Zileuton mechanism

A

effects not immediate

inhibits enzyme that converts arachidonic acid into leukotrienes

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18
Q

Zileuton pharmacokinetics

A

PO, rapid absorption

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19
Q

Zileuton Adverse effects

A

Liver injury, possible hepatitis

Neuropsychiatric effects

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20
Q

montelukast: three indications

A

1) prophylaxis and maintenance in asthma

2) prevention of exercise-induced bronchospasm

3) relief of allergic rhinitis

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21
Q

montelukast mechanism

A

high affinity for leukotriene receptors

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22
Q

montelukast pharmacokinetics

A

PO rapidly absorbed

Metabolised in liver

Excreted in bile

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23
Q

Mast cell Stabilizer drug

A

Cromolyn

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24
Q

Cromolyn

A

Inhalation agent that suppresses bronchial inflammation

Prophylaxis in patients with mild to moderate asthma

Used when glucocorticoids cause problems
- not as effective as glucocorticoids

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25
Q

Mech of Cromolyn

A

Stabilizes mast cells
- prevent release of histamines
- inhibits eosinophils and macrophages

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26
Q

cromolyn pharmacokinetics

A

administrered by nebulizer
excreted unchanged in urine

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27
Q

Cromolyn therapeutic uses

A

Maximal effects take weeks to develop

prophylaxis for season allergy attacks

Administer 10-15 prior to exercise

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28
Q

Cromolyn Adverse effects

A

safest of all anti-asthma medications

29
Q

preparation , dosage and administration of cromolyn

A

adults/children: 20 mg 4x/day

maintenance= lowest effective dose

30
Q

Monoclonal Antiboides

A

form newest drug for airway inflammation

non are approved for first-line agents and for management of acute asthmatic episodes

31
Q

IgE Antibody Antagonist

A

Omalizumab

32
Q

three categories of monoclonal antibodies

A

1) IgE Antibody Antagonist

2) Interleukin-5 Antagonist

3) Interleukin-4 Receptor Alpha Antagonist

33
Q

Omalizumab

A

Second-line agent

34
Q

Omalizumab mechanism of action

A

-forms complexes with IgE in blood
= reduced available IgE
= limits availability of allergen to trigger release of histamine

35
Q

therapeutic use of Omalizumbab

A

when asthma is allergy-related
or can’t be controlled by glucocorticoid

only for patients with a specific allergen

36
Q

Omalizumab pharmacokinetics

A

administration: subQ injection

absorbtion: slow- peak levels in 7-8 days

half life 26 days

37
Q

Omalizumab adverse effects

A

variety: injection site reaction, upper respiratory infection, sinusitis, pharyngitis

life-threatening anaphylaxis occurs rarely

38
Q

preparations, dosage, administration omalizumab

A

powder reconstituted in sterile water
- then sub Q

dose and dosing interval determined by body weight and total serum IgE

39
Q

Interleukin-5 Receptor Antagonist

A

Benralizumbab

40
Q

Interleukin-5 (IL-5)

A

responsible for differentiation and maturation of eosinophils

41
Q

mechanism of action Benralizumab

A

IL-5 receptor antagonists bind to IL-5 receptor
= inhibit
= reduced production of eosinophils

42
Q

Therapeutic Use Interleukin-5 Receptor Antagonist

A

Restricted: only for severe eosinophilic asthma

43
Q

Adverse effects of Benralizumab

A

SubQ injection: site of reaction, back pain

hypersensititivity

44
Q

Interleukin-4 Receptor antagonist

A

Dupilumab

45
Q

IL-4

A

Inflammatory cytokine that binds to many cells involved in inflammation

46
Q

Mech of Dupilumab

A

its a monoclonal antibody (made in lab) that binds to IL-4 receptor
= decreased inflammatory response

Used for eosinophilic asthma

47
Q

Dupilumab Adverse effects

A

SubQ injection site reaction, conjectivitis

48
Q

Phosphodiesterase-4 inhibitor

A

Roflumilast
- approved for sever chronic COPD with a primary chronic bronchitis component

49
Q

mechanism of Roflumilast

A

PDE4 breaks down cAMP

There fore PDE-4-inhibior = increased cAMP

cAMP reduces inflammation by suppressing cytokine release and decreasing pulmonary infiltration of neutrophils and other WBC

50
Q

therapeutic use of roflumilast

A

not first line

prophylaxis for severe chronic bronchitis patients

51
Q

adverse effects of roflumilast

A

the greatest concern is anxiety and depression to suicidal behavior

52
Q

Bronchodilators

A
  1. Beta2- Andrenergic Agnosits
  2. Anti-Cholinergic
53
Q

Beta 2- Andregnergic Agonists

A

Inhaled are most effective for acute bronchospasm and preventing EIB

54
Q

Beta2- Andrenergic Agonists mechanism

A

Drug activates beta2-andrenergic recptors
- activated receptors in lung = bronchodilator

  • limited role in suppressing histamine release
55
Q

administration of bronchodilators

A

PO- long-term control, long-lasting, fixed schedule
- for asthma must be combined with glucocorticoid

INHALED
- short-acting (3-5hr)
- take before exercise to prevent attack

56
Q

Anti-Cholinergic Drug name

A

Ipratropium

  • approved only for COPDme
57
Q

mechanism of Anti-cholinergic

A

blocks bronchi muscarinic receptors
= reduced bronchoconstriciton

  • effects within 30 seconds, persist 6 hr
58
Q

Therapeutic use Ipratropium

A

Inhalation
- system effects are minimal

59
Q

Adverse effects of Ipratropium

A

dry mouth, irritation of pharynx

60
Q

Combination Drugs

A

1) Glucocorticoid/ Long-Acting Beta2 Agonists

2) Beta2 adrenergic agonist/ Anticholinergic Combination

61
Q

Glucocorticoid/Long-Active Beta 2 Agonsit Combination

A
  • Anti inflammatory benefits of glucocorticoids
  • bronchodilation of beta2 agonists
  • for pt not controlled with inhaled glucocorticoid
  • not first line
  • black box
62
Q

Beta 2- adrenergic agonist/ anticholinergic combination

A
  • beta 2 agonist : bronchodilation by stimulating adrenergic receptors
  • anticholinergic: brochodilation by blocking cholinergic receptors
63
Q

Classification of asthma severity

A

1) intermittent
2) mild persistant
3) moderate persistent
4) severe persistent

64
Q

what is severity of asthma classification based upon

A

impairment- quality of life, functional capacity

risk- adverse events

65
Q

initial therapy for acute/severe exacertbation

A
  • oxygen: hypoxemia
  • systemin glucocorticoid: inflammation
  • nebulized high-dose SABA: airflow obstruction
  • Nebulized Ipratropium (anti-cholinergic): further reduce airflow obstruction
65
Q

Stepwise managing asthma

A

1) inhaled SABA (short-acting beta agonist) as needed

2) ling-term control med = generally inhaled glucocorticoid

3) dosage increased or another medication is added

4) after a period of sustained control, move down a step is tried

65
Q

drugs for acute/severe exacerbations goal of drugs

A
  • relieve hypoxia
  • relieve airway inflammation
  • relieve airway obstruction
  • normalize lung function
66
Q

cause of exercise-induced bronchospasm (EIB)

A

loss of heat or water from lung

67
Q

preventing EIB

A

inhale SABA (preferred)

Cromolyn (mast-cell stabilizer prophylactically

hlsc final (12 decks)

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