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Pharmacotherapy 1 > Airway & Lung Diseases > Flashcards

Airway & Lung Diseases Flashcards

1
Q

Asthma stats

A

affects ~10% population (39.5 million ppl)

  • higher in blacks
  • higher in females
  • higher in children
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2
Q

Pathophysiology of Asthma

A

-chronic inflammatory disease involving episodes of REVERSIBLE airway obstruction (reversibility distinguishes asthma from COPD)

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3
Q

Asthma characterized by:

A

A) Chronically inflamed airways

B) Airway Hyperreactivity

C) Airway Smooth Muscle Hypertrophy

D) IgE-Mediated Immune Response

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4
Q

A) Chronically Inflamed Airways

A
  • epithelial damage
  • mucosal edema
  • inflammatory cell infiltration (eosnophils, lymphocytes, neutrophils)
  • mediator release
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5
Q

Mediator Release

A
  • PGs : bronchoconstriction
  • Leukotrienes C4/D4 : bronchoconstriction, airway hyperreactivity
  • Platelet Activating Factor: airway hyperreactivity
  • Histamine: no role
  • Adenosine: bronchoconstriction, mast cell activation -Cytokines: IL5-eosinophil recruitment, IL4-IgE production
  • Tryptase: airway inflammation (PAR2: protease activated receptors)
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6
Q

What evidence could you provide that argues against histamine or PGs being important mediators of asthma?

A

Antihistamine and COX-inhibitors do not help in asthma!

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7
Q

B) Airway Hyperreactivity

A

-increased responsiveness to a variety of stimuli (bronchoconstrictors, irritants, exercise)

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8
Q

C) Airway smooth muscle hypertrophy

A

-increase bronchial reactivity

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9
Q

D) IgE mediated immune response

A
  • mast cells have an important role in asthma
  • continual exposure to antigen
    • inflamed airways
    • increased airway reactivity
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10
Q

Hygiene hypothesis

A

in early life, decreased exposure to infections + increased antibiotic use + decreased exposure to noxious pulmonary stimuli causes a change in immune system development

  • decreased Th1 response (infection fighting)
  • increased Th2 response (allergic diseases, asthma)
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11
Q

Bronchoconstriction precipitated by variety of stimuli:

A

A) Environmental (house dust mite, animal dander, tobacco smoke, air pollutants, ozone)

B) Occupational (grain dust, red cedar)

C) Drugs (propanolol, aspirin)

D) Exercise

Reducing exposure–>less asthmatic episodes

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12
Q

Asthmatic episodes divided into:

A

A) Early response

B) Late Response

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13
Q

Early Response

A

bronchoconstriction occurring immediately after exposure

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14
Q

Late Response

A

bronchoconstriction occurring hours after exposure

  • hyperreactivity lasts for several weeks
  • may relate to release of mediators from infiltrating inflammatory cells and the time it takes for them to infiltrate
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15
Q

Asthmatic episodes exacerbated by:

A
  • viral respiratory infection
  • rhinitis
  • sinusitis
  • cigarette smoke
  • pollution
  • gastroesophageal reflux
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16
Q

Clinical features of Asthma

A
  • wheezing, chest tightness
  • non-productive cough
  • episodic airflow obstruction
  • increased airway reactivity to non-specific stimuli
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17
Q

Episodic airflow obstruction

A

A) During remission: PFTs may be normal

B) During partial remission: no clinical signs, but may see decreased pulmonary function from peak flow meter (bronchoconstriction without knowing it, flow meter can detect the bronchoconstriction without them knowing it is present)

18
Q

Diagnosis

A

PFTs (pulmonary function test):

  • decreased expiratory flow rate, FEV-1, FVC
  • increased residual volume, FRV
  • decreased ability to exhale, causes increased residual volume
19
Q

Diagnosis

A

2) Bronchial provocation tests:
- airway hyperreactivity correlates with severity of asthma
- PFTs performed before and after admin. of incrementally-increased conc. of bronchoconstrictor aerosol (e.g. methacholine)
- the more hyperreactive your airways are, the more likely you are to have bronchoconstriction

20
Q

COPD epidemiology

A

-affects ~6% of population of industrialized countries -15 million people in USA diagnosed in 2011

21
Q

COPD prevalence

A
  • whites,black>hispanic
  • women>men
  • older>younger
  • Smoker>non-Smoker, and former smoker>non-smoker
  • less education>more education

–unemployed>employed

22
Q

COPD stats

A

-3rd leading cause of death in US -2nd leading cause of disability -# of death declining, but declining more in men than in women -$43 billion cost of COPD–> significant impact on healthcare

23
Q

COPD Pathophys.

A

-COPD is a common preventable and treatable disease characterized by persistent airflow limitation that is USUALLY PROGRESSIVE and assoc. w/ enhanced chronic inflammatory response in airways and the lung to noxious particles or gases

=syndrome of progressive, NON-REVERSIBLE airflow limitation caused by chronic inflammation of the small airways and alveoli

24
Q

COPD pathophys. con’t

A
  • umbrella term that encompasses chronic bronchitis, emphysema, and small airway diseases (asthma affects central airways more)
  • Primary cause is the EXPOSURE TO PARTICLES, e.g. TOBACCO SMOKE
25
Q

COPD features

A

A) Chronically inflamed Airways

B) Imbalance between Protease and Anti-Protease Activity

C) Airway Remodeling

D) Pulmonary Vascular Changes

26
Q

A) Chronically Inflamed Airways

A
  • inflammatory cell infiltration of the (small) airways and alveoli (macrophages, lymphocytes, neutrophils)
  • mucus hypersecretion
  • decreaed ciliary motility
  • mediator release
27
Q

B) Imbalance Between Protease and Anti-Protease Activity

A
  • Imbalance in favor of proteolysis –> remodeling –> emphysema
  • Proteolytic activity correlates with disease severity
28
Q

C) Airway Remodeling

A
  • bronchiolar scar tissue development
    • airway narrowing/fixed airway obstruction
    • airflow limitation NOT FULLY REVERSIBLE (vs. asthma)
  • emphysema
    • centrilobular (respiratory bronchiole destrcution)
    • panlobular (respiratory bronchioles and alveolar ducts/sacs destruction)
      • decreased tethering of airways
      • decreased gas exchange
29
Q

D) Pulmonary Vascular Changes

A
  • endothelial cell dysfunction (changes gas exchange)
  • inflammatory cell infiltration of vessel wall (changes gas exchange)
  • smooth muscle hypertrophy (changes flow)
30
Q

Pathophysiological Consequences

A
  • mucus hypersecretion + ciliary dysfunction –> increased cough & sputum
  • airway narrowing + peripheral airway destruction–> expiratory flow limitation (irreversible)
  • inflammatory cell infiltration + mucus hypersecretion–> expiratory flow limitation (reversible)
  • peripheral airway remodeling –> impaired elastic recoil –> increased lung volume (gas gets trapped in lungs)
  • airway obstruction + pulmonary vascular changes –> hypoxia/hypercapnia
31
Q

Based on pathophys. consequences, what would happen to FEV-1 and residual volume in a patient with moderate COPD?

A

* Residual volume increases * FEV decreases

32
Q

Risk Factors

A

A) Noxious Particles/gases * tobacco smoke * environmental particulates * occupational dusts & chemicals

B) Genetic * AAT-deficiency (genetically predisposed to emphysema) (important inhibitor of neutrophil elastase and serine proteases)

C) Older age >40yrs

D) Poor socioeconomic status

E) Lower Respiratory Tract infections

F) Low Birth weight * poor nutrition of fetus, small lungs, start life w/ reduced lung function

33
Q

Pathogenesis

A

1) Inhaled Noxious stimulus

* epithelial cell damage

* alveolar macrophage activation cytokine release fibroblast activation (–>fibrosis)

* mac, neutrophil recruitment

34
Q

Pathogenesis

A

2) Macrophage & Neutrophil Activation

* ROS/Protease release

* CD8- cell recruitment

* Tissue damage/remodeling–>emphysema

* goblet cell hyperplasia–> mucus

35
Q

Macrophages and neutrophils in COPD pts (i) have reduced capacity to phagocytize bacteria and (ii) are less responsive to the effects of corticosteroids.

A

Bacteria in the airways are trapped in the mucus, have a lot of mucus and have less ability to clear the mucus, the inflammatory cells have less capacity to phagocytize bacteria, and steroids have less capacity in their anti-inflammatory effects in patients with COPD as opposed to asthma patients

36
Q

Co-morbities

A

* lung cancer

* cardiovascular disease

* depression

* skeletal muscle wasting

* osteoporosis

37
Q

Clinical features

A

* Persistent Dyspnea

* Chronic Cough

* Sputum Production

* Wheezing/Chest Tightness

38
Q

Diagnosis

A

Suspect COPD in a pt > 40 if:

* persistent or progessive dyspnea (difficult gas exchange)

* chronic cough

* chronic sputum production

* history of exposure to risk factors (smoking)

* family history of COPD

39
Q

Diagnosis

A

spirometry (PFT) required to validate clinical diagnosis of COPD

40
Q

Spirometry diagnosis

A

* decreased expiratory flow rate, FEV-1, FVC, FEV-1/FVC

* increased residual volume, FRC

41
Q

What are the differences in the causes of decreased FEV-1 in COPD vs asthma? (hint think about causes of flow limitation)

A
  • Drop in FEV-1 in asthma is due to bronchoconstriction
  • Drop in FEV-1 in COPD is due to REMODELING plus bronchoconstriction (COPD pt’s FEV will not look like a normal pt’s FEV b/c there is remodeling and thus not fully reversible, over time, the non-bronchodilator sensitive component will get worse and FEV will decrease more over time)

Pharmacotherapy 1 (4 decks)

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