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Pulmonology > Porth - Obstructive Pulmonary Disorders > Flashcards

Porth - Obstructive Pulmonary Disorders Flashcards

1
Q

Bronchiectasis - Definition

A
  • Uncommon type of COPD - Permanent dilation of the bronchi and bronchioles (widened airways)

– ^^ Caused by destruction of muscle & elastic supporting tissue as result of cyclical Infection & Inflammation

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2
Q

Is Bronchiectasis a Primary Disease?

A

No! Occurs 2ndary to persistent infection or obstruction

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3
Q

What was Bronchiectasis associated with in the past?

A

-Used to follow a Necrotizing Bacterial Pneumonia that complicated measles, pertussis, influenza, or TB.

– Has decreased due to Immunizations & Antibiotic use

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4
Q

Pathogenesis of Bronchiectasis

A
  1. Obstruction
  2. Chronic Persistent Infection

*Both damage bronchial walls =’s weakening and dilation

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5
Q

2 Presentations of Bronchiectasis:

A
  1. Local obstructive process - involving a lobe or segment of lung
  2. Generalized/Diffuse process - involving much of both lungs
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6
Q

Localized Bronchiectasis

A

Causes: Tumors, Foreign Bodies, Mucous Plugs =’s cause atelectasis & infection

* Blocks drainage of bronchial secretions

** Local area determined by the site of obstruction or infection

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7
Q

Generalized Bronchiectasis

A

Causes: Inherited impairments of host mechanisms; or acquired disorders that introduce bad organisms into airways — Including: Cystic Fibrosis; Lung Infection (TB, lung abscess); congenital/acquired immunodeficient states; exposure to toxic gases * Usually Bilateral ** Most commonly affects lower lobes

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8
Q

Bronchiectasis Clinical Features

A
  • Atelectasis - Small airway obstruction - Diffuse Bronchitis –Recurrent bronchopulmonary infection: Coughing; production of copious amount of foul-smelling/purulent sputum; hemoptysis — Weight loss & anemia can occur
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9
Q

Bronchiectasis Manifestations

A

*Similar to those in Chronic Bronchitis & Emphysema – Marked Dyspnea – Cyanosis

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10
Q

Bronchiectasis & Clubbing of the Fingers

A
  • More common in moderate to advanced cases

*Not commonly seen in other types of obstructive lung diseases

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11
Q

Bronchiectasis Diagnosis & Treatment

A

Diagnosis: -Hx

  • Imaging Studies: evident on Chest Radiographs, High-resolution CT scanning of chest

Treatment: - Early recognition & treatment of infection are key!

– Postural drainage & Chest PT — Remove mucous &good hydration

*Patients benefit from many of the rehabilitation & treatment measures used for Chronic Bronchitis & Emphysema

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12
Q

Emphysema - A Type of COPD!

A

Characterized by: Loss of lung elasticity & abnormal enlargement of air spaces distal to terminal bronchioles w/ destruction of alveloar walls & capillary beds - Enlargement of air spaces & destruction of lung tissue

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13
Q

Emphysema

Enlargement leads to…

A

Hyperinflation of lungs and increase Total Lung Capacity (TLC)

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14
Q

Emphysema

Two Causes

A
  1. Smoking = incites lung injury
  2. deficiency of alpha1-antitrypsin (an enzyme that protects the lung from injury) - Genetic factors
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15
Q

Emphysema Results from….

A
  • Breakdown of Elastin and other alveolar wall components by enzymes (proteases) that digest proteins
  • Things like smoking cigarettes calls all these inflammatory cells into the lungs, resulting in an influx of these digestive enzymes.
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16
Q

Emphysema & alpha1-antitrypsin deficiency

A

1% of COPD cases

  • Found in younger folks w/ emphysema (generally diagnosed before age of 40)

– More common in Scandinavians

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17
Q

Chronic Bronchitis - A Type of COPD!

A

Airway obstruction of the major and small airways.

  • Increased mucous production; obstruction of small airways, chronic productive cough
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18
Q

Chronic Bronchitis is found most commonly in…

A

Middle-aged men & associated with common irritation from smoking & recurrent infections

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19
Q

Chronic Bronchitis & Clinical Dx requires…

A
  • History of chronic productive cough that has persisted for at least 3 consecutive months in at least 2 years

– In general, cough has been present for many years w/ increase in exacerbations that produce sputum

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20
Q

Chronic Bronchitis

Earliest Feature

A

Hyper secretion of mucus in the large airways

  • associated with hypertrophy of submucosal glands in the trachea & bronchi
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21
Q

Chronic Bronchitis

What’s going on in the Large & Small Airways?

A
  • Large airways: Mucus hyper-secretion/submucosal hypertrophy
  • Small airways: Increase in goblet cells & excess mucous production
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22
Q

Chronic Bronchitis + Viral and Bacterial Infections

A
  • Common in Chronic Bronchitis

– Thought to be a result of, not a cause of CB

— Probably help in maintaining CB

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23
Q

COPD: Emphysmea & Chronic Bronchitis

Clinical Features

A
  1. Insidious Onset
  • Fatigue
  • Exercise intolerance
  • Sputum Production
  • SOB

* Productive cough more common in the morning

**Dyspnea is more severe as disease progresses

24
Q

COPD: Emphysmea & Chronic Bronchitis

Late Stages

A

Recurrent respiratory infections & Chronic Respiratory failure

*Death occurs during an exacerbation of illness associated with infection & resp. failure

25
Q

COPD: Emphysmea &Chronic Bronchitis

Manifestations: “Pink Puffers”

A

*Predominant Emphysema

**Lack of Cyanosis

***Use of Accessory Muscles

****Pursed Lipped-Breathing

26
Q

COPD: Emphysmea

“Pink Puffers” & their Barrel Chests

A
  • Lung elasticity lost & Lungs Hyper-inflated
    • Lungs often collapse during expiration =’s air gets trapped in alveoli and lungs increasing AP-dimension of chest

*Dramatic decrease in breath sounds

**Diaphragm fatigue & Acute Respiratory Failure

27
Q

COPD: Chronic Bronchitis

Manifestations: “Blue Bloaters”

A

*Predominant in Chronic Bronchitis

  • Reference to:
    • Cyanosis
    • Fluid Retention due to Right-Sided Heart Failure :(
28
Q

COPD: Emphysmea &Chronic Bronchitis

Is the Obstruction of Airflow worse on Inspiration? or Expiration?

A

Expiration!

  • Increased work of breathing & Decreased Effectiveness
29
Q

COPD: Emphysmea & Chronic Bronchitis Late Stage COPD (pt. 1)

A
  • As disease progresses: Expiration is prolonged & Wheezes and Crackles can be heard - Labored Breathing, even at Rest - “Tri-poding” - Pursed Lip Breathing
30
Q

COPD: Emphysmea & Chronic Bronchitis Late State COPD (pt. 2)

A
  • Unable to maintain normal blood gases – Resulting in: Hypoxemia, hypercapnia, cyanosis *V/Q imbalance!
31
Q

COPD: Emphysmea & Chronic Bronchitis Severe Hypoxia

A
  • Arterial PO2 levels below 55mmHg – Vasoconstriction of pulmonary vessels & even less gas exchange in lungs — Can cause Polycythemia (red blood cell production) — Increases Right Ventricle work, hence the right-sided heart failure
32
Q

COPD: Emphysmea & Chronic Bronchitis Diagnosis

A
  • History & Physical crucial - PFTs – FVC & FEV1 decreased - Chest Radiographs - Lab tests
33
Q

COPD: Emphysmea & Chronic Bronchitis Treatment

A
  • Depends on Disease Stage – Smoking Cessation — Maintain & Improve Pulmonary Fxning: Pulmonary Rehabilitation (breathing exercises) — Avoid those who are sick as to not get respiratory infections —- Vaccines —– Medications: Bronchodialators: Inhaled B2-agonists; anticholinergic, adrenergic agents; oral Theophylline (measure blood levels) – Oxygen Therapy
34
Q

Emphysema 2 commonly recognized types: Centriacenar & Panacinar

A
  1. Centriacinar (or Centrilobular): Most common; seen in male smokers; most common in upper lungs

– Affects bronchioles in the central part of the respiratory lobule

— Initial preservation of alveolar ducts & sacs

  1. Panacinar: More common in alpha1-antitrypsin deficiency; more common in lower parts of lungs
    - Initial involvement of the peripheral alveoli & later extends to involve more central bronchioles
35
Q

Obstructive Airway Disorders:

Asthma

A
  • A chronic disorder of the airways that causes episodes of airway obstruction due to bronchial smooth muscle hyperreactivity and airway inflammation.
  • Episodes are usually reversible (compare to COPD)
36
Q

Asthma

Some Factoids

A
  • Affects ~5% of population
  • Prevalance of asthma has increased
  • Disease management has gotten better over the years
    • Decreased hospitalizations & mortality rates
37
Q

Asthma

Characterized by…

A
  • Variable recurring symptoms
  • Airflow obstruction
    • Episodic wheezing
    • Difficulty breathing
    • Tight chest
    • Cough (worse in PM and AM)
  • Bronchial hyperresponsiveness
38
Q

Asthma

2 Types

A
  1. Extrinsic: Type I hypersensitivity (atopic) response to extrinsic antigen
  2. Intrinsic: Initiatied by non-immune mechanisms:
  • Resp. Tract Infections
  • Exercise
  • Ingestion of Aspirin
  • Emotions
  • Bronchial Irritants (i.e. smoke)
39
Q

Asthma

The Common Denominator!

A

An exaggerated hypersensitivity response to a variety of stimuli.

Contributors:

  • Inflammatory cells & epithelial damage
  • Mucus hypersecretion
  • Smooth muscle hypertrophy
  • Blood vessel proliferation

*Genetic & Evironmental factors play a part!

40
Q

Asthma

Extrinsic (Atopic)

A
  • Initiated by Type I hypersensitivity reaction
    • Exposure to antigen or allergen
  • Childhood/Adolescent onset
  • Family Hx
41
Q

Asthma

Extrinsic Asthma

A
  • These folks often have other allergic d/o:
    • Hay Fever
    • Urticaria
    • Eczema
  • Year-round allergens:
    • House mites
    • Cockroach allergens
    • Animal Danders
    • Alternaria (fungus)
      ​
42
Q

Asthma

Extrinsic Asthma & Response Mechanisms

Early/Acute Phase

A
  • Early/Acute phase:
    • 10-20 minutes to develop
    • Caused by: IgE-mediated release of mediators from sensitized mast cells
  • Bronchospasm
  • Mucosal Edema
  • Increased Mucous Secretions
  • Can usually be Inhibited or Reversed by:
    • Bronchodilators (B2-agonists)
43
Q

Asthma

Extrinsic Asthma & Response Mechanisms

Late Phase

A
  • Develops 4-8 hours after exposure
    • ‘Vicious cycle of exacerbations’
  • Epithelial cell injury w/ decrease mucociliary fxn and accumulation of mucus.
    • Release of inflammatory mediators
  • Increased vascular permability & edema
  • Increased airway responsiveness
  • Bronchospasm
  • Edema
  • Reduced clearance of respiratory tract secretions
  • Increased airway responsiveness
  • Can lead to airway remodeling
44
Q

Asthma

Instrinsic (nonatopic)

Triggers

A
  • Resp. Tract Infections
  • Exercise
  • Hyperventilation
  • Cold air
  • Drugs & Chemicals
  • Hormonal changes & emotional upsets
  • Air-bourne pollutants
  • Gastro-esophageal reflux
45
Q

Asthma

Intrinsic (nonatopic)

A

Cause epithelial damage and stimulate the production of IgE antibodies directed toward the viral antigens.

46
Q

Asthma

Intrinsic

Exercise & Cold Enviroments

A
  • Exercise: Hyperventilation & airway physiology change play a role
    • Increased ventilation rate challenges ability of airways to condition air before reaching the alveoli
  • Cold Environment: Exaggerates response of exercise
    • Warm-up
    • Wear a mask over mouth & nose
47
Q

Asthma

Intrinsic

Inhaled Irritants

A
  • Tobacco smoke/strong odors
    • Induce Bronchospasm
      • Irritant receptors & vagal reflex
  • Children exposed =’s increases severity of asthma
  • Occupational Asthma: fumes, gases, chemical dusts
48
Q

Asthma

Intrinsic

Aspirin

A
  • Clinical Triad:
    • Nasal Polyps
    • Chronic Rhinosinusitis
    • Bronchial Asthma
  • Mechanism of reaction is unclear, but due in part to:
    • Acidic metabolism issues
  • If you have this condition… avoid Aspirin!
49
Q

Asthma

Clinical Features

A
  • Range of Symptoms:
    • Wheezing
    • Tight Chest
    • Acute Immobilizing Attacks
  • May be spontaneous, or in response to a trigger
  • Nocturnal Asthma: Worse @ night
50
Q

Asthma

Clinical Features

A
  • Bronchospasm
    • Causes Airways to narrow
  • Edema of Bronchial Mucosa
  • Mucus plugging
  • Prolonged expiration
    • Decreased FEV and PEF
51
Q

Asthma

Clinical Features

Prolonged Attack

A
  • Lung hyperinflate
  • Decreased Inspiratory Reserve Capacity & Forced Vital Capacity
  • More energy required to overcome tension & maintain ventilation
  • Dyspnea & Fatigue
  • V/Q mismatch
    • Hypoxemia & Hypercapnia
  • Increased work demands of the Right Heart
52
Q

Asthma

Manifestations

A
  • Mild attack:
    • Chest tightness
    • Resp. Rate increase w/ prolonged expiration
    • Mild wheezing (w/w/o cough)
  • Severe attack:
    • Accessory muscle use
    • Distant breath sounds
    • Loud Wheezing
  • Progresses:
    • Fatigue
    • Moist skin
    • Anxiety/Apprehension
    • Decreased breath sounds, decreased wheezing, Ineffective cough
      • THIS IS NOOOOOOO GOOD!
53
Q

Asthma

Diagnosis

A
  • Hx
  • PE
  • Lab findings
  • Pulmonary Fxn Studies
    • Spirometry
    • Small portable meters measuring PEF are available
      • Measure ‘personal best’
54
Q

Asthma

Treatment

A
  • Control contributing factors & exposures
    • Education
    • Annual Flu Vaccine
    • Desensitization program
  • Drugs:
    • Bronchodialtor
    • Anti-inflammatory drugs
    • SABAs
      • Relax bronchial muscles
      • Prompt relief
    • Anticholinergic agents
      • Blook cholinergic receptors
      • Reduce intrinsic vagal tone that causes constriction
        • Bronchodilation
      • Longer onset of action
  • Long-term Meds:
    • inhaled corticosteroids*
      • Most effective!
    • long-acting bronchodialtors
    • cromolyn,
    • leukotriene pathway inhibitors
    • theophylline
55
Q

Asthma

Severe Asthma

A
  • A sub-group
  • High medication dose
  • Persistant
  • Requires continuous high-dose inhaled or oral corticosteroids
  • More fatal attacks/rapid deterioration
56
Q

Asthma in Children

A
  • Most common cause of childhood ER visits, hospitalizations, missed school days
  • 80% of children are Symptomatic before age 6
  • Increasing globally
  • Ig-E related reaction
    • Assc. w/ Virus (RSV previously)
    • Environmental exposures
  • Often see symptoms at night
  • Step-wise approach to treatment
    • Inhaled corticosteroid are 1st-line
    • Nebulizer therapy for very youngins’

Encourage active participation in recreational activities

Pulmonology (5 decks)

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