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GI/Pulm > Pulm Pharm > Flashcards

Pulm Pharm Flashcards

1
Q

Drug deposition of inhaled drugs: ideal size

A

1-5 micrometers= ideal for smaller airways
> 10 micrometers= deposited in lung, oropharynx
< 0.5 micrometers= inhaled and exhaled without deposition

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2
Q

Quick relief drugs (asthma)

A

Take when you have symptoms:

  • Short acting bronchodilators
  • High dose oral or IV medications
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3
Q

Controller (asthma)

A

Controller= take every day

  • anti-inflammatory
  • mediator antagonists
  • longer-acting bronchodilators
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4
Q

MOA of Beta-2 agonists

A

Binds receptor–> increased adenylyl cyclase–> increased cAMP–> PKA–> decreased Ca+2–> bronchorelaxation

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5
Q

Selective Beta-2 agonists

A

Clinical role:

  • Acute symptom relief: Bronchorelaxation, Minimal tachyphylaxis
  • Bronchoprotection: Known triggers (cold air, allergens), Attenuates with repeated use
  • No antiinflammatory properties
  • Oral administration should be avoided

Short acting: Albuterol= workhorse drug

  • First choice quick relief for asthma
  • As needed ~every 4 hours
  • Higher doses used in acute attack

Long acting: salmeterol, formoterol

  • Every 12 hours
  • Theoretical concerns of tachyphylaxis; NOT for immediate relief
  • Should NOT be administered without inhaled steroids

AEs: tachycardia, tremor, nervousness
- hypokalemia: CV disease with diuretic use= highest risk–> potential arrhythmia (COPD population)

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6
Q

Albuterol

A 
Workhorse drug for asthma (short-acting)
Beta-2 agonist
- First choice quick relief for asthma
- As needed ~every 4 hours
- Higher doses used in acute attack
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7
Q

Salmeterol/formoterol

A

Long-acting asthma drug- beta-2 agonist

  • Every 12 hours
  • Theoretical concerns of tachyphylaxis; NOT for immediate relief
  • Should not be administered without inhaled steroids
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8
Q

Corticosteroid use in asthma

A

MOA: Bind cytoplasmic receptor associated with HSP 70 & 90 and immunophilin (target of cyclosporine)

  • Translocation to nucleus to serve as transcription factor
  • Widespread cellular effects

Effects:

  • decrease lymphocyte number
  • decrease cytokine release and production by lymphocytes and macrophages
  • decrease endothelial cell adhesion molecules (ICAM-1)
  • Eosinophil apoptosis
  • decrease prostaglandin and leukotriene C4
  • decrease fibroblast proliferation

AEs: immunosuppresion, gastric ulcers, osteoporosis, muscle wasting, cataracts (blocking immune response)

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9
Q

Inhaled corticosteroids for asthma/COPD

A

Long term administration: Mainstay of asthma treatment

  • Use in ALL except mildest disease
  • No immediate bronchorelaxation

COPD usage: decreases exacerbations but does not change mortality/lung function

Side effects mild and dose related:

  • HPA suppression–minimal
  • Cataracts–posterior subcapsular
  • Growth velocity in children: Titrate dose to control of disease
  • Bone mineral density: significant decrease only at higher doses
  • Fractures: no increased risk, but poor data
  • Pneumonia—mild risk in COPD patients

Local side effects:

  • Dysphonia, thrush: independent of type of steroid
  • Strategies to avoid: rinse mouth, spacer device

Treatment side effects typically better than severe disease in children

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10
Q

Parenteral (IV or IM) corticosteroids for asthma

A
  • Used in severe attacks
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11
Q

Oral corticosteroids for asthma

A

Used in acute exacerbations: excellent bioavailability

  • Long term use for asthma and COPD associated with significant toxicity
  • Short term use very effective
  • Preferred to increasing dose of inhaled steroid
  • Initiate therapy early in exacerbation
  • Use appropriate dose, usually for ~ 5-10 days
  • Monitor for decline in symptoms
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12
Q

Anticholinergics for asthma: MOA

A

CNS, autonomic ganglia, heart, GI system, sweat glands, GU tract, eye
- 5 receptor subtypes

Lung receptors:

  • M3 receptor: smooth muscle and mucous glands
  • Antagonism of receptor inhibits bronchoconstriction by histamine, bradykinin, eicosanoids and decreases production of secretions (anesthesia)
  • Jimson weed (atropine) smoked in India to treat asthma
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13
Q

Pharmacokinetics/pharmacodynamics of anticholinergics

A
  • Only 1% of inhaled dose absorbed
  • MDI or nebulization
  • Scheduled (not symptom driven) dosing

Ipratropium (Atrovent)
- Maximal response 30-90 min, duration 4-6 hr

Tiotropium (Spiriva)

  • Slower onset, duration of action 24 hours
  • M1 and M3 selective
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14
Q

Clinical use of inhaled anticholinergics

A
  • Effect depends upon vagal tone
  • Minimal effect on mucociliary clearance
  • First line therapy in COPD (after smoking cessation)
  • Adjunct in asthma
  • Side effects mild: Dry mouth
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15
Q

Leukotrienes in asthma

A

Eicosanoid family: increase or attenuate inflammation

  • C4, D4= mediators of inflammation
  • Derived from arachidonic acid
  • Basis for aspirin-sensitive asthma: aspirin shunts arachidonic acid into leukotriene pathway
  • Bind to CysLT receptor–> effector reaction

In Asthma: Potent effectors of airway obstruction; Leukotrienes cause:

  • Bronchial constriction
  • Vasodilation
  • Leukocyte chemotaxis
  • Edema

Leukotriene drugs in asthma= receptor antagonists or synthesis inhibitors

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16
Q

Montelukast

A

Leukotriene receptor antagonist (modifiers)
- q day; Very safe

  • Add-on controller agent in asthma
  • Pediatrics: oral, steroid sparing
  • Treats allergic rhinitis
  • Heterogenous response
  • NO ROLE in COPD

Side effects:
- Churg-Strauss vasculitis (associated with severe asthma, responds to corticosteroids)

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17
Q

Zafirlukast

A

Leukotriene receptor antagonist (modifiers)

  • BID; Mild Cytochrome P450 inhibition
  • Very safe
  • Add-on controller agent in asthma
  • Pediatrics: oral, steroid sparing
  • Heterogenous response
  • NO ROLE in COPD

Side effects:
- Churg-Strauss vasculitis (associated with severe asthma, responds to corticosteroids)

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18
Q

Zileuton

A

Leukotriene synthesis inhibitor

  • BID sustained release
  • LFT monitoring needed
  • Also blocks LTB4
  • Limited use
19
Q

Cromolyn Sodium

A

AKA “Mast cell stabilizer” or cromone

Modes of action may include

1) Inhibition of mediator release from mast cells
2) ↓ chemotaxis
3) sensory nerve effects (↓ cough, neuropeptide release)

Safety: Excellent
Efficacy: Modest

Cromones: used in allergic asthma, QID dosing limits compliance

20
Q

Theophylline

A

MOA:
Methylxanthine
Inhibits cyclic nucleotide phosphodiesterase enzymes, cAMP and cGMP, bronchodilation
Competitive inhibitor of adenosine receptor, which may mediate bronchospasm

*Efficacy probably due more to antiinflammatory and bronchoprotective effects than bronchodilatory effects

Side effects: Caffeine derivative:

  • within therapeutic index: nervousness, insomnia, dyspepsia
  • Dose-dependent toxicity: nausea, emesis, tachyarrhythmias, seizures
Notes:
Third line agent in asthma
Minor role in management of COPD
Requires therapeutic monitoring
BUT…Inexpensive and oral (3rd world use)
21
Q

Roflumilast

A

Specific phosphodiesterase-4 isotype: better side effect profile than theophylline

Indicated for severe COPD

  • Reduces exacerbation rates
  • Not for acute bronchorelazation
  • Inhibits PDF-4–> GI effects, weight loss
22
Q

Omalizumab

A

Recombinant humanized anti-IgE antibody
MOA: Binds circulating IgE, but does not activate cell bound IgE

Administered by subcutaneous injection every 2-4 weeks
~$1,000 / month
Only for use in treatment-resistant asthma

23
Q

Order of treatment of Chronic Asthma with increasing symptoms

A
  1. Short-acting beta-2 agonists
  2. Inhaled corticosteroids
  3. Theophylline, leukotriene modifiers, tiotropium, long-acting Beta-2 agonists
  4. Oral steroids
24
Q

Acute asthma exacerbation treatment

A

Mild worsening of symptoms
- Double dose of inhaled steroid

Outpatient exacerbation
- 2 mg/kg prednisone day (max 60) for two days, followed by 1 mg/kg for 2-4 more days (single dose or split twice/day)

Inpatient severe exacerbation
- 1 mg/kg methylprednisolone q6 for at least one day, then wean to oral ~2 mg/kg q day

25
Q

Principles of COPD therapeutics

A

First line:

  • Smoking cessation: Only way to prevent further irreversible damage
  • Scheduled use of inhaled anticholinergic +/- long acting beta-2 Adrenergic agonists
  • Immunization: pneumococcus and influenza
  • Theophylline: Provides symptom relief but no mortality benefit

Corticosteroids

  • Oral helpful in acute exacerbations, but should be avoided on a chronic basis
  • Inhaled corticosteroids decrease number of exacerbations, but do not change FEV1 or parenchymal destruction
  • Antibiotics for COPD exacerbation-probably effective
  • Leukotriene modifiers- No indication

Inhaled 100% O2 (if less than 55%)

26
Q

COPD exacerbation treatment

A

Inhaled anticholinergics
Inhaled beta2 agonists
Oral or IV steroids
Oral antibiotics modestly effective

27
Q

Pulmonary hypertension

A

Idiopathic= uncommon, poor prognosis

Secondary, caused by:

  • Cardiac abnormalities
  • Obstructive sleep apnea
  • Chronic pulmonary embolism
  • Pulmonary parenchymal problems-COPD
  • Connective tissue disorders
  • HIV
  • Sickle cell disease
28
Q

Sildenafil

A

PDE5 localized to lung
Antagonism causes: Vasodilation, Apoptosis
Increased cardiac contractility
First line for mild/moderate Pulmonary HTN
TID

29
Q

Tadalafil

A

PDE5 localized to lung
Antagonism causes: vasodilation, apoptosis
Increased cardiac contractility
First line for mild/moderate pulmonary HTN
qday

30
Q

Bosentan

A

Treatment for pulmonary HTN

MOA: Antagonism of endothelin receptors (A and B)
- Causes Vasodilatation, Antiproliferative

Stabilizes smooth muscle proliferation
Teratogenic, alters metabolism of contraceptives
$35,000 year

31
Q

Ambrisentan

A

Treatment for pulmonary hypertension

MOA: Antagonism of endothelin receptors (A and B): Vasodilatation, Antiproliferative

ET-A1 receptor specificity
Liver toxicity
Teratogenic
Limited access distribution program

32
Q

Epoprostenol (prostacyclin)

A

Used in severe primary pulmonary HTN

MOA:

  • Decreases pulmonary vascular resistance and mean pulmonary arterial pressure
  • Decreases platelet aggregation and smooth muscle proliferation
  • Lengthens time to transplantation in PPH
  • Can be used with anticoagulants
  • Reserved for severe disease

Limitations:

  • Short half life requires continuous infusion
  • High incidence of infection from chronic indwelling catheter
  • Expensive

Other drugs: Treprostinil (SubQ), Iloprost (inhaled)

33
Q

Calcium channel blockers for Pulmonary HTN

A

Requires testing to predict response
Nifedipine or diltiazem
Therapy initiated very slowly

34
Q

Alternatives for Pulmonary HTN treatment

A

Calcium channel blockers
Systemic anticoagulation for warfarin
Oxygen

35
Q

Nicotine

A

Physiologic effects complex:
- Stimulatory receptors
- Inhibitory receptors
CNS: stimulation, which is responsible for the “pleasure-reward” effect
Cardiovascular: short term–
- vasoconstriction, tachycardia, elevated blood pressure
GI: increased tone and motor activity

36
Q

Smoking cessation strategies

A

Behavioral
Nicotine replacement (patch, gum)
Bupropion (Zyban)
Varenicline (Chantix)

37
Q

Nicotine replacement patch

A

Dosing variable: 5-22 mg
- doubles cessation success rates at one year
Often combined with short acting forms (gum, nasal spray)

On 24 hours: “Doc, first thing I do in the morning is smoke”

On only while awake: Prevent insomnia, nightmares

38
Q

Nicotine nasal spray

A

0.5 mg/spray (usual dose 1-3)
quick absorption mimics cigarette delivery
Expensive
May foster nicotine dependence

39
Q

Nicotine gum/lozenge

A

2-4 mg

  • chew gum until tingling is noted, park, and then chew again
  • unpleasant taste
40
Q

Nicotine inhaler

A

Buccal nicotine absorption

  • mimics hand-mouth habit of cigarettes
  • 95% absorption in buccal mucosa
  • expensive; complicated; moderate to poor response rates
41
Q

Varenicline

A

MOA: partial agonist to alpha-4 beta-2 nicotinic acetylcholine receptor subtypes

  • Reduces withdrawal and reward of nicotine
  • Dose titrated up over a week before quit date
  • Duration of therapy 12-24 weeks

Adverse effects:

  • Nausea in up to 30%
  • Worse with nicotine or replacement Tx
  • Withdrawals in studies not worse than bupropion
  • Suicidal ideation risk warning from FDA
  • 56 tablets $180
42
Q

Buproprion

A

Antidepressant: used for smoking cessation and mood disorders
MOA: Modulates NE and DA transport

Side effects:

  • Blood pressure increases
  • possible seizure risks (enhanced in anorexics)
  • Neuropsychiatric adverse events
Use:
7 days before quit date
- 6 months use (up to 12 months)
- Can be used with nicotine
- 60 tablets ~ $80
43
Q

Rimonabant

A

Blocks cannabinoid receptors

GI/Pulm (7 decks)

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