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Respiratory Medicine Midterm > The Lung Part 3 > Flashcards

The Lung Part 3 Flashcards

1
Q

Other forms of emphysema

A
  • Associated with lung overinflation or focal emphysematous change
  • compensatory hyperinflation
  • Obstructive overinflation
  • Bullous emphysema
  • Interstitial emphysema
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2
Q

Compensatory hyperinflation

A
  • used to designate dilation of alveoli in response to loss of lung substance elsewhere
  • best exemplified by hyper expansion of residual lung parenchyma following surgical removal of a diseased lung or lobe
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3
Q

Obstructive overinflation

A
  • Lung expands because air is trapped within it
  • cuase: subtotal obstruction of airways by tumor or foreign object
  • Another example=congenital lobar overinflation in infants, probably resulting from hypoplasia of bronchial cartilage and sometimes associated with other congenital cardiac and lung abnormalities
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4
Q

Overinflation in obstructive lesions occurs because:

A

either:

1) obstructive agent acts as ball valve, allowing air to enter on inspiration while preventing its exodus on expiration OR
2) because COLLATERALS bring in air behind the obstruction
- these collaterals consist of pores of Kohn and other direct accessory bronchioloalveolar connections (canals of Lambert)
- Obstructive overinflation can be life-threatening emergency, because affected portion distends sufficiently to compress remaining lung

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5
Q

Bullous emphysema

A
  • Large subpleural blebs or bulle (spaces greater than 1 cm in diameter in distended state) that can occur in any form of emphysema
  • These localized accentuations of emphysema occur near apex, sometimes near old tuberculous scarring
  • rupture of bullae may give rise to pneumothorax
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6
Q

Interstitial emphysema

A
  • Entrance of air into connective tissue storm of lung, mediastinum, or subcutaneous tissue produces interstitial emphysema
  • Alveolar tears in pulmonary emphysema provide avenue of entrance of air into stroma of lung, but rarely, chest wounds that allow entry of air or fractured ribs that puncture the lung substance underlie this disorder
  • Alveolar tears are usually caused by rapid increases in pressure within alveolar sacs, such as occurs when there is combination of coughing and bronchiolar obstruction
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7
Q

Who is most at risk for interstitial emphysema

A

-Premature children on positive pressure ventilation and adults who are being artificially ventilated are most at risk

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8
Q

Chronic bronchitis

A
  • persistent cough with sputum production for at least 3 months in at least 2 consecutive years, in absence of any other identifiable cause
  • common in habitual smokers and inhabitants of smog-laden cities, chronic bronchitis is one end of spectrum of COPD with emphysema being the other (most patient lie somewhere in between with features of both)
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9
Q

When chronic bronchitis persists for years,

A

-accelerates decline in lung function, lead to for pulmonale and heart failure or cause atypical metaplasia and dysplasia of respiratory epithelium, providing rich soil for cancerous transformation

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10
Q

Pathogenesis of chronic bronchitis

A
  • primary/initiating factor is exposure to noxious inhaled substances like tobacco smoke (90% are smokers) and dust from grain, cotton, and silica
  • Mucus hyper secretion
  • Inflammation
  • Infection
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11
Q

Mucus hyper secretion in chronic bronchitis

A
  • earliest feature of chronic bronchitis is hyper secretion of mucus in large airways, associated with hypertrophy of submucosal glands in trachea and bronchi
  • involves mediators like histamine and IL-13
  • increase in goblet cells in small airways (small bronchi and bronchioles) leading to excessive mucus production that contributes to airway obstruction
  • Both submucosal gland hypertrophy and increase in goblet cells are protective reactions against tobacco smoke or other pollutants (e.g., sulfur dioxide and nitrogen dioxide)
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12
Q

Inflammation in chronic bronchitis

A
  • inhalants cause cellular damage eliciting acute and chronic inflammatory responses involving neutrophils, lymphocytes, and macrophages
  • Long standing inflammation and fibrosis of small airways (small bronchi and bronchioles 2-3 mm) can lead to chronic airway obstruction–also seen in emphysema and common denominator in COPD
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13
Q

Infection in chronic bronchitis

A

-Infection does NOT initiate chronic bronchitis but is probably significant in maintaining it and may be critical in producing acute exacerbations

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14
Q

Ways that smoking predisposes to chronic bronchitis

A
  • damages airway lining cells leading to chronic inflammation
  • interferes with ciliary action of respiratory epithelium, preventing clearance of mucous and increasing risk of infection
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15
Q

Clinical features of chronic bronchitis

A
  • persistent cough productive of sparse sputum
  • For many years, no other respiratory functional impairment present but eventually, dyspnea on exertion develops
  • With time and continued smoking, other elements of COPD seen including hypercapnia, hypoxemia, mild cyanosis (blue bloaters)
  • Long standing severe chronic bronchitis leads to cor pulmonale and cardiac failure
  • Death may also result from further impairment of respiratory function due to superimposed infections
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16
Q

Morphology of chronic bronchitis

A
  • Grossly there is hyperemia, swelling, and edema of mucous membranes accompanied by excessive mucous or mucopurulent secretions
  • sometimes heavy casts of secretions and pus fill bronchi and bronchioles
  • mild chronic inflammation of airways (predominantly lymphocytes) and enlargement of mucus-secreting glands of trachea and bronchi
  • number of goblet cells increase slightly, but major change is in size of mucous glands (HYPERPLASIA)–seen by thickness of mucous gland layer to thickness of wall bw epithelium and cartilage (Reid index)
  • Reid index (normally 0.4) is increased in chronic bronchitis usually in proportion to severity and duration of disease
  • Bronchial epithelium shows squamous metaplasia and dysplasia
  • marked narrowing of bronchioles caused by mucous plugging, inflammation, and fibrosis
  • In the most severe cases, there may be obliteration of lumen due to fibrosis (bronchiolitis obliterates)
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17
Q

Asthma

A

-chronic disorder of the conducting airways, usually caused by an immunological reaction, which is marked by episodic bronchoconstriction due to increased airway sensitivity to a variety of stimuli; inflammation of the bronchial walls; and increased mucus secretion

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18
Q

Asthma symptoms

A
  • recurrent episodes of wheezing, breathlessness, chest tightness, and cough, particularly at night and/or early morning
  • associated with bronchoconstriction and airflow limitation that is at least partly reversible, either spontaneously or with treatment
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19
Q

status asthmaticus

A
  • acute severe asthma
  • can be fatal
  • patients have had a long history of asthma
  • between attacks may be completely asymptomatic
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20
Q

Asthma may be characterized as

A
  • Atopic (allergen sensitization and immune activation in patients with allergic rhinitis or eczema) or non-atopic (no evidence of allergen sensitization)
  • In both types, episodes can have diverse triggers like resp infections (esp viral), irritant exposure (smoke, fumes), cold air, stress and exercise
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21
Q

Early onset allergic asthma associated with TH2 helper T cell inflammation

A
  • seen in half of asthma patients
  • responds well to corticosteroids
  • no consensus as to definitions and diagnostic criteria
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22
Q

Asthma classified according to agents or events that trigger bronchoconstriction

A
  • seasonal
  • exercise induced
  • drug induced (aspirin)
  • occupational asthma
  • asthmatic bronchitis in smokers
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23
Q

Atopic asthma

A
  • IgE mediated (type I) hypersensitivity reaction
  • begins in childhood, triggered by env allergens like dusts, pollen, cockroach or animal dander and foods which act in synergy with pro inflammatory env cofactors (resp viral infections)
  • common FH of asthma
  • positive skin test–immediate wheal and flare run
  • also diagnosed by high serum total IgE levels or by evidence of serum radioallergosorbent tests (RAST) which detect presence of IgE Ab specific for allergens
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24
Q

Non-atopic asthma

A
  • NO allergen sensitization
  • NEGATIVE skin tests
  • LESS common FH of asthma
  • common triggers=Resp infections due to viruses (rhinovirus, parainfluenza virus, RSV)
  • Other contributors to airway inflammation and HS: smoking, sulfur dioxide, ozone, nitrogen dioxide
  • may be triggered by harmless things like cold/exercise
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25
Q

Drug-induced asthma–Aspirin sensitive asthma

A
  • Aspirin sensitive asthma (uncommon) occurs in people with recurrent rhinitis and nasal polyps–sensitive to small doses of aspirin and other NSAID and experience both asthmatic attacks and urticaria
  • Asprin and NSAIDS triggers asthma by inhibiting COX leading to decrease in PGE2 which normally inhibits pro inflammatory mediators like LTB4, C4, D4 and E4 which play central role in aspirin induced asthma
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26
Q

Occupational asthma

A
  • triggered by fumes (epoxy resins, plastics), organic and chemical dusts (wood, cotton, platinum), gases (toluene) or other chemicals (formaldehyde, penicillin products)
  • very small quantities required to induce attack
  • mechanisms vary: type I reaction, direct liberation of bronchoconstrictor substances and HS runs of unknown origin
27
Q

Pathogenesis of Asthma

A
  • Atopic asthma caused by TH2 and IgE response to environmental allergens in genetically predisposed individuals
  • Airway inflammation causes airway dysfunction through release of inflammatory mediators and through remodeling of airway wall
  • As disease gets severe, see local secretion of GFs which induce mucus gland hypertrophy, smooth muscle proliferation, angiogenesis, fibrosis and nerve proliferation
28
Q

TH2 responses, IgE and inflammation in asthma

A
  • TH2 cells secrete cytokines that promote inflammation and stimulate B cells to produce IgE and other Abs
  • Cytokines: IL-4 stimulates production of IgE; IL-5 activates eosinophils; IL-13 stimulates mucus secretion from bronchial submucosal glands and promotes IgE production by B cells
  • T cells and epithelial cells secrete chemokines that recruit more T cells and eosinophils, exacerbating rxn
  • IgE binds to Fc receptors on submucosal mast cells and repeat exposure to allergen triggers mast cells to release granule contents and produce cytokines, and other mediators, collectively inducing the EARLY PHASE rxn and late phase rxn
29
Q

Early reaction in asthma

A
  • dominated by bronchoconstriction, increased mucus production, vasodilation and increased vascular permeability
  • Bronchoconstriction triggered by direct stimulation of sub epithelial vagal (parasympathetic) receptors through both central and local reflexes triggered by mediators produced by mast cells and other cells in rxn
30
Q

Late phase reaction in asthma

A
  • dominated by recruitment of leukocytes, esp eosinophils, neutrophils and more T cells
  • TH2 cells are dominant T cell type involved in disease but other T cells also contribute like TH17 (IL-17 producing) cells which recruit neutrophils
31
Q

Mediators whole role in bronchospasm in asthma clearly supported by efficacy of pharmacologic intervention are:

A

1) Leukotrienes C4, D4, and E4 cause prolonged bronchoconstriction and increased vascular permeability and increased mucus secretion
2) acetylcholine: released from intrapulmonary parasympathetic nerves which can cause airway smooth muscle constriction by directly stimulating muscarinic receptors

32
Q

Second group of agents that are present in asthma (at “scene of crime”) but play minor role on the basis of lack of efficacy of potent antagonists or synthesis inhibitors

A
  • Histamine: potent bronchocontstrictor
  • PGD2: bronchoconstrictor and vasodilation
  • Platelet-activating factor: causes aggregation of platelets and releases serotonin from granules
  • these may be important in certain chronic or non-allergic asthmas
33
Q

third group of agents in asthma for whom specific antagonists or inhibitors are not available (“suspects”)

A
  • IL-13/IL-4 signal transduction pathways
  • IL-13 monoclonal Abs and IL-4 receptor Antagonists in progress
  • Other targets include IL-1, TNF, IL-6, chemokine (eotaxin aka CCL11), neuropeptides, NO, bradykinin, endothelins
34
Q

Genetic susceptibility of asthma

A

-susceptibility to atopic asthma is multigenic and often associated with increased incidence of other allergic disorders like allergic rhinitis (hay fever) and eczema

35
Q

Susceptibility locus for asthma located on chromosome

A
  • 5q near gene cluster encoding cytokines IL-3, IL-4, IL-5, IL-9, and IL-13 and the IL-4 receptor
  • Polymorphisms in the IL-13 HAVE STRONGEST and most consisten associations with asthma or allergic disease
36
Q

_____ are linked to production of IgE Abs against some antigens like ragweed pollen

A

HLA class II alleles

37
Q

Polymorphisms in the gene encoding _____ is linked to increased proliferation of bronchial smooth muscle cells and fibroblasts, contributing to bronchial hyperreactivity and subepithelial fibrosis

A

ADAM33–a metaloproteinase

38
Q

____ are associated with differential in vivo airway hyper-responsiveness and in vitro response to B-agonist stimulation

A

B2-adrenergic receptor gene variants

39
Q

____ gene variants are associated with atopy, elevated total serum IgE and asthma

A

IL-4

40
Q

Other things associated with asthma

A
  • variants in members of mammalian family of chitinases, enzymes that cleave chitin, a polysaccharide contained in many human parasites and the cell walls of fungi
  • increased serum levels and lung expression of YKL-40 (chitinase-like glycoprotein expressed and secreted by a variety of cells) correlated with disease severity, airway remodeling and decreased pulmonary function
41
Q

Asthma is a disease of what kind of societies? Why?

A
  • industrialized societies where the majority of people live in cities
  • Because industrialized envs have many airborne pollutants that act as allergens to initiate TH2 response
  • Also, city life limits exposure of very young children to certain Ags, esp microbial antigens, and exposure to such Ags protects against asthma and atopy–even more apparent if exposure occured during pregnancy
  • called hygeine hypothesis–has spurred trials of probiotics and putative allergens given to children to decrease their risk of later developing allergies
42
Q

Infections and asthma

A
  • Infections themselves not trigger for asthma but children with aeroallergen sensitization who develop lower respiratory tract viral infections (rhinovirus type C, resp syncytial virus) have 10-30-fold increased risk of developing persistent and/or severe asthma
  • Both bacterial and viral infections associated with acute exacerbations
43
Q

Airway remodeling in asthma

A
  • repeated bouts of allergen exposure and immune reactions result in structural changes in bronchial wall leading to airway remodeling
  • include hypertrophy and hyperplasia of bronchial smooth muscle, epithelial injury, increased airway vascularity, increased subepithelial mucus gland hypertrophy and deposition of subepithelial collagen
44
Q

Morphology of asthma

A
  • status asthmaticus–lungs are distended by overinflation and contain small areas of atelectasis
  • OCCLUSION OF BRONCHI AND BRONCHIOLES by thick, tenacious mucus plugs, which often shed epithelium
45
Q

Asthma–Characteristic finding in sputum or bronchoalveolar lavage specimens is

A
  • Curschmann spirals–can result from extrusion of mucus plugs from subepithelial mucous gland ducts or bronchioles
  • also present are eiosiniphils and Carcot-Leyden crystals–composed of eosinophils protein called galectin-10
46
Q

Airway remodeling in asthma–histological findings

A
  • Thickening of airway wall
  • Subbasement membrane fibrosis (due to deposition of type I and type III collagen)
  • Increased vascularity
  • Increase in size of submucosal glands and number of airway goblet cells
  • Hypertrophy and/or hyperplasia of bronchial wall muscle
  • acute airflow obstruction attributed to muscular bronchoconstriction, acute edema and mucus plugging; airway remodeling also contributes to chronic irreversible airway obstruction
47
Q

Asthma clinical course

A
  • classic acute asthmatic attack lasts upto several hours
  • In some, chest tightness, dyspnea, wheezing and coughing (with or without sputum production) are present at a low level constantly
  • status asthmaticus–most severe form–lasts for days and even wweeks causing airflow obstruction so extrme that marked cyanosis or even death can occur
48
Q

Asthma diagnosis

A

-Based on demonstration of increase in airflow obstruction (from baseline), difficulty with exhalation (prolonged expiration, wheeze), peripheral blood eosinophilia and finding of eosinophils, Curschmann spirals and Carcot-Leyden crystals in sputum (esp in atopic asthma)

49
Q

Asthma treatment and prognosis

A

-more disabling than lethal; can maintain productive life
Therapy based on severity of disease
-50% remits in adolescence but returns in adulthood in many patients
-variable decline in baseline lung function

50
Q

Bronchiectasis

A
  • disorder in which destruction of smooth muscle and elastic tissue by chronic necrotizing infections leads to permanent dilation of bronchi and bronchioles
  • now uncommon bc of better control of lung infections
51
Q

Bronchiectases associated with what conditions?

A
  • Congenital or heriditary conditions
  • Infections
  • Bronchial obstruction
  • Rheumatoid arthritis, SLE, IBD, COPD and posttransplantation (chronic lung rejection and chronic graft vs. host disease after bone marrow transplant)
52
Q

Bronchiectasis–congenital and heriditary causes

A
  • Cystic fibrosis
  • Intralobar sequestration of the lung
  • Immunodeficiency states
  • Primary ciliary dyskinesia
  • Kartagener syndromes
53
Q

Bronchiectasis–infectious causes

A
  • necrotizing pneumonia caused by bacteria, viruses or fungi

- may be single severe episode or recurrent infections

54
Q

Bronchiectasis–obstructive causes

A
  • tumor
  • foreign bodies
  • mucus impaction
  • in each of these cases, bronchiectasis is localized to obstructed lung segment
55
Q

1/4 to 1/2 of bronchiectasis–cause is

A

IDIOPATHIC!!

56
Q

Pathogenesis of brochiectasis

A
  • obstruction and infections major associated conditions–both necessary to develop bronchiectasis
  • obstruction impairs normal clearing mechanism resulting in pooling of secretions distal to obstruction and secondary infection and inflammation
  • severe infections of bronchi lead to inflammation with necrosis, fibrosis and eventually dilation of airways
57
Q

Cystic fibrosis and bronchiectasis pathogenesis

A
  • Both obstruction and infection
  • primary defect in ion transport leads to defective mucociliary action and airway obstruction by thick viscous secretions–sets stage for chronic bacterial infections which cause damage to aiway walls; destruction of smooth muscle and elastic tissue leads to bronchi dilation and obliteration of smaller bronchioles due to fibrosis (bronchiolitis obliterans)
58
Q

Primary ciliary dyskinesia

A
  • Autosomal recessive
  • ciliary dysfunction due to defects in ciliary motor proteins leads to retention of secretions and recurrent infections that lead to bronchiectasis
  • ciliary fnx needed for proper rotation of organs in chest and abdomen
  • have of patients with primary ciliary dyskinesia have Karatagener syndrome marked by situs inversus or partial lateralizing abnormality associated with bronchiectasis and sinusitis
  • lack of ciliary activity interferes with bacterial clearance, predisposies sinuses and brochi to infection and affects cell motility during embryogenesis leading to situs inversus
  • Males with this=INFERTILITY bc of sperm dysmotility
59
Q

Allergic bronchopulmonary aspergillosis

A
  • occurs in patients with asthma and cystic fibrosis who develop periods of exacerbation and remission that may lead to proximal bronchiectasis and fibrotic lung disease
  • results from HS rxn to aspergillus fumigatus
  • sensitization to aspergillus in allergic host leads to activation of TH2 helper T cells which recruits eiosinophils and leukocytes
  • characterized by high serum IgE, Abs to aspergillus, intense airway inflammation with eosinophils and formation of mucus plus
60
Q

Bronchiectasis morphology–gross

A
  • Affects LOWER lobes bilaterally, esp airways that are vertical, most severe in more distal bronchi and bronchioles
  • if bronchiectasis is due to tumors or aspiration, it is localized to single lung segment
  • airways dilated sometimes up to 4x normal size and can be followed almost to pleural surface bc of dilation (in normal lungs, bronhioles cannot be followed by eye beyond 2-3 cm from plerual surface)
  • dilated bronchi cystic, with mucopurulent secretions
61
Q

Bronchiectasis histological findings

A
  • vary with chronicity
  • full blown case–intense, acute and chronic inflammatory exudation within walls of bronchi and bronchioles associated with desquamation of lining epithelium and extensive areas of ulceration; may be pseudostratification of columnar cells or squamous metaplasia; sometimes necrosis destroys bronchial or bronchiolar walls and forms lung abcesses
  • Fibrosis of bronchial and bronchiolar fibrosis develop in more chronic cases, leading to varying degrees of subtotal or total obliteration of bronchiolar lumens
62
Q

Bacteria associated with bronchiectasis

A
  • Staph, strep, pneumoccoci, enteric organisms, anaerobic and microaerophilic bacteria and Haemophilus influenzae and pseudomonas aeruginosa
  • In allergic bronchopulmonary aspergillosis, few fungal hyphae seen on special stains within mucoinflammatory contents of dilated segmental bronchi
  • In late stages fungus may infiltrate bronchial wall
63
Q

Clinical course of bronchiectasis

A
  • causes severe persistent cough, foul smelling, sometimes bloody sputum, dypnea and orthopnea in severe cases and sometimes hemoptysis which may be massive
  • episodic symptoms and precipitated by upper respiratory tract infections or new pathogenic agents
  • cough especially frequent in morning bc change in position causes collections of pus and secretions to drain into bronchi
  • Obstructive respiratory insufficiency can lead to marked dyspnea and cyanosis but new txs has doubled life expectancy so cor pulmonale, brain abcesses and amyloidosis are less frequent complications than in past

Respiratory Medicine Midterm (17 decks)

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