L18 Asthma and COPD Flashcards

1
Q

Risk factors of asthma?

A
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2
Q

Signs/Symptoms of Asthma

A

Symptoms of Asthma: Cough, Wheeze, Shortness of Breath, Chest Tightness

Signs of Asthma: Hyperexpansion of chest cavity, prolonged expiratory time, expiratory wheezing, use of respiratory muscles

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3
Q

What allows asthma to be differentiated from COPD?

A

Asthma’s reversibility w/ broncho dilator allows it to be differentiated from COPD

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4
Q

What is Atopy and what is its significance?

A

Atopy is the tendency to produce an exaggerated immunoglobulin E immune response to otherwise harmless substances in the environment

  • Presence of atopy makes asthma more likely than COPD
  • Determines sensitivity to indoor allergens
  • Serologic testing:

IgE- elevations indicate the presence of allergic sensitization

radioallergosorbent test (RAST)

Allergen skin testing– Guides interventions to reduce exposure

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5
Q

Pathology of Asthma?

A

Reduction in airway luminal diameter

  • excessive mucus production
  • thick basement membrane
  • airway inflammation
  • bronchial hyper-responsiveness

Interactions between CD4 T Cells and B Cells => IgE Synthesis

Airway obstruction caused by some combination of

– Airway smooth-muscle constriction

– Inflammation of the bronchi

– Abnormal smooth-muscle contractility or Excess smooth-muscle mass

– Eosinophil influx

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6
Q

Th1 versus Th2 Phenotype of Asthma?

A
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7
Q

Asthma Treatment?

A

Reduction in bronchial inflammation when treated => still too many goblet cells

relaxation of airway smooth muscle (bronchodilators)

suppression of airway inflammation (anti-inflammatory drugs)

newer medication (dual effects)

– leukotriene modifiers

– Anti IgE therapy

drug combinations– inhaled corticosteroids combined with long-acting β-adrenergic agonists

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8
Q

Characteristics of COPD?

A

COPD is Chronic airflow obstruction due to chronic bronchitis and/or pulmonary emphysema

Primarily caused by cigarette smoking

Some patients with asthma develop poorly reversible airflow limitation

– indistinguishable from patients with COPD

– for practical purposes are treated as asthma

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9
Q

Diagnosis of COPD?

A

Diagnosis of COPD considered in any patient who has the following symptoms:

– cough

– sputum production or

– dyspnoea or

– history of exposure to risk factors for the disease (tobacco smoking++)

The diagnosis is confirmed with spirometry

Assessment of COPD severity

– spirometry

– functional dyspnoea

– body mass index = weight (Kg)/ height2 (m)

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10
Q

COPD Pathology? (4 Compartements impacted)

A

COPD => pathological changes in 4 different compartments of the lungs:

  • central airways
  • peripheral airways
  • lung parenchyma
  • pulmonary vasculature
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11
Q

Physiological Abnormalities in COPD

A

Physiological abnormalities in COPD

– mucous hypersecretion

– ciliary dysfunction

– airflow limitation

– hyperinflation

– gas exchange abnormalities

pulmonary hypertension: destroys capillary beds => secondary hypertension from increased PVR

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12
Q

Smoking’s Contribution to COPD

A

Smoking is the main risk factor for COPD + Other inhaled noxious particles and gases

Oxidative stress from free radicals in tobacco smoke => Imbalance of proteinases and anti-proteinases in the lungs

– Free radicals impair activity of anti-proteases

– ⇑ Proteases enzymes damages the lungs

Inflammatory response in the lungs

Irritation of the mucous membrane

– bronchitis

– Increased mucous secretion

– ball and valve obstruction

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13
Q
A
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14
Q

Chornic Bronchitis Pathogeneis?

A

known as “blue bloaters

bronchi inflammation => eventual fibrosis/scarring

Pathogenesis

• inflammation of the wall of bronchi and bronchioles

• increased mass of mucous glands=> excessive production of mucus and sputum

• Airways become narrowed => ⇓ airflow

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15
Q

Clinical Diagnostic Criteria fro Chornic Bronchitis

A

Cough + sputum (productive cough) for 3 months/year over 2 years

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16
Q

Complications of Chronic Bronchitis?

A

Hypercapnia

Respiratory acidosis

Hypoxemia

Polycythemia (elevated hemoglobin levels)

CO2 retention

=> pulmonary artery vasoconstriction

=> pulmonary hypertension

=> cor pulmonale

=> right heart failure

17
Q

Emphysema Pathogenesis

A

pink puffer

Alveoli (air sacs) enlargement and destruction => minimal inflammation, some fibrosis

Pathogenesis

Destruction of lung tissue distal to the terminal bronchiole (acinus) => permanent enlargement of the air spaces

Destruction of the alveolar walls

=> destruction of the capillary bed

=> increased pulmonary vascular resistance

=> pulmonary hypertension

Increased Lung compliance => Reduced elasticity, Hyperinflation, Poor lung mechanics

18
Q

What is the role of Alpha-1 Anti Trypsin Deficiency?

What do people w/o it develop?

What can cure it?

A

Alpha 1 Antitrypsin (AAT) is a protease inhibitor “lung protector” produced by liver and immune cells

In absence of ATT => neutrophil elastase not inhibited

=> unregulated breakdown of elastin

=> increased alveolar compliance

In the absence of AAT, patients develop: emphysema (PANACINAR) and liver cirrhosis

Liver transplantation can cure the condition if diagnosed in childhood

19
Q

Two Types of Emphysema?

A

Centrilobular (most common)

damage is limited to the central part of the lobule or acinus (upper lobes most affected)

– preserved peripheral alveolar ducts and alveoli

Smokers

Panacinar (rare)

destruction of the entire lobule

Genetic: Alpha-1-anti-trypsin deficiency (protease inhibitor) =>increased destruction of elastin

IVDU: can be seen in talc IV drug abuse and in Ritalin use

20
Q

Clinical Signs of Emphysema (3)

A

Barrel-shaped chest

– increased antro-posterior diameter

– sternum pushed forward

– widened subcostal angle

Accessory muscles of respirations

hyperactive

prominent (e.g.,sternomastoids) (gasping for breath)

Intercostal spaces

widened

Horizontal ribs

21
Q

Complications of COPD?

Emphesema vs. Bronchtis?

A

Infection

– Pneumonia

– bronchiectasis

– tuberculosis (due to decreased local immunity of the lung)

Pulmonary hypertension

– in bronchitis

• fibrosis involving lung capillaries.

– in emphysema

  • destruction of capillary beds in alveolar walls
  • compression of the alveolar septa by trapped air

Pneumothorax

– rupture of bullae into the pleura

– air in the pleural cavity

– push the lung towards the mediastinum

– lung collapse with mediastinal

22
Q

COPD Causes of Death?

A

COPD Causes of Death

Respiratory failure: ventilation, perfusion, and diffusion are all affected with resultant severe hypoxaemia and hypercapnia

Core pulmonale: Right-sided heart failure due to pulmonary hypertension induced by lung lesion

Lung cancer: squamous metaplasia (chronic bronchitis) & smoking are risk factors for lung cancer

23
Q

Management of COPD?

A

Established COPD is not curable but controllable

Smoking cessation -Most important factor in slowing down the progression of COPD

Pharmacotherapy

Bronchodilators: β2 agonists, M3 antimuscarinics, leukotriene antagonists

=> relax the smooth muscles of the airway allowing for improved airflow