Obstructive lung diseases

Dr Neelam Doshi

Year2 Semester 4 23/05/2017

1600-1800
 Learning objectives
1. Review the respiratory tract structure, epithelium and
pulmonary function tests.

2. Outline the conditions that cause obstructive lung

disease.

3. Discuss underlying aetiology, pathogenesis and

pathology.

4. Correlate pathology with clinical features and

complications.
C Structure of lower respiratory tract
O
N
D
U
respiratory unit=acinus
C
T
Gas exchange area
I lobules
N
G

Z
O
N
E
R
E
S
P
I
R
A
T
O
R
Y

Z
O
N
E
Histology Respiratory epithelium
Respiratory Pressures
Described relative to atmospheric pressure (Patm) ~ 760 mmHg
Negative respiratory pressure (<760 mmHg)
Positive respiratory pressure (>760 mmHg)

PTpul l
Prevents
lung collapse

Pip
Maintains
pull on
lungs

(Ppul)
Determines
direction of air flow
 Pressure changes during
RESPIRATION
0 (=to Atm press) at end of expiration, then negative to atmosphere as no air, then
as inspires Ppul rises to 1 at end of insp. as max tidal vol. then as Exp starts P pul
falls back to attm =0 as expires all air out

Pip has to be
high at exp. as
it pushes the
lung tissue to
expire air out
Pulmonary volumes and capacities

4 volumes 4 capacities

With forced
inspiration

Forced insp +
Forced exp
 Spirometry measuring
ventilatory function
Volume / time curve (spirogram)
VC, FVC, FEV1 calculated manually

Flow / volume loop

More commonly used

Portable spirometers
Computerized, automatic

Peak flow meters

PEF
Patient use
 Factors affecting pulmonary
ventilation
1. Airway resistance ( AWR)
Length, radius and cross sectional area of the airways
Resistance inversely proportional to airway diameter
Normally insignificant
Highest in medium sized bronchi and low in alveoli
Alveoli thou smallest in dia but cross sectional area is largest when combine all of the alveoli
Processes that increases resistance lead to n arrowing of airways
INTRINSIC EXTRINSIC

Broncho-constriction
Due to parasympathetic stimulation
Caused by Irritant chemicals /pollution Mucus/Tumor/Foreign body

2. Lung compliance
i. Elastic recoil of chest wall (2/3 rd) and lung tissue ( 1/3 rd)
ii. Surfactant
 Airways Flow and resistance
Resistance to airflow
Greatest in early part of
expiration/inspiration
Medium sized bronchioles
muscle contraction
oedema in walls
mucus in lumen
Inflammation
Tumor in lumen
Obstructive Airway Disorders (OAD)
Characterised by airway obstruction which results in
reduced airflow, particularly during expiration
More force is required to expel air (resistence to
expiratory air flow), so emptying is slower and longer
( Deep long breaths)
Spirometer tests (PFT): Obstructive pattern
decreased FEV1, FVC unchanged , decreased FEV1 / FVC ratio ( 25-
50%)
Wheezing is a common sign
E.g. Asthma, Chronic Bronchitis, Emphysema, Cystic fibrosis
Acute or Chronic OR Localised or Diffuse
Usually co exist
Prototypes of Obstructive Lung Disease

COPD
3 2

Loss of elastic Airway narrowing

recoil

4 BRONCHIECTASIS
Airway disorders

or

or

 PFT Obstructive disorders

PEFR High flow

period: chest
wall force
Low constant
low:
AWR/small
TLC RV
Flo

alveoli
w

Volume

PIFR

Almond/Witch
Cashew=concave hat=convex

Pierce, R and Johns, DP, Spirometry: The Measurement

and Interpretation of Ventilatory Function in Clinical
Practice
 Case 1
Kae is a 13 year old girl has been experiencing an episodic
increase in breathing difficulties associated with wheeze and
tight ness of the chest. Episodes are short-term and semi-
regular and more in springs/autumns.
the timing ,frequency of the symptoms,
and triggering or exacerbating factors
What more to ask? Environmental association at home/school
 Asthma
Paroxysmal and reversible obstructive disorder of the
airways
Narrowing of airways and hyper responsiveness to various
triggers SOB, wheeze, chest tightness, and coughing
Extrinsic-Atopic and Intrinsic-Adult onset, Non atopic
Infections usually
Mucus plugs and enlarged bronchial mucus glands
Pathogenesis: Many cells and cellular elements play a role
Mast cells, Eosinophils, T lymphocytes, macrophages, neutrophils, and
epithelial cells
IL 4/5 , IgE antibodies (TH 2)
Early morning/late night
bronchial hyper-responsiveness to a variety of stimuli
Ref: National Asthma Management Handbook 2006, National Asthma Council, Australia)
Pathophysiology
pictorial

Type 1
hypersensitivity
Pathophysiology summary
Goblet cell hyperplasia in bronchus in asthma
 Chronic obstructive airway
disorders-Irreversible
Chronic bronchitis clinical entity
Persistent productive cough for at-least 3 consecutive mo. over 2
consecutive years
Persistent obstruction of BRONCHI and largely irreversible due to mucus
secretion and airway thickening as a result of chronic inflammation

Emphysema functional/morphological entity

Abnormal permanent enlargement of the airways and destruction of
alveolar walls voluminous lungs with increased compliance
obstruction in emphysema is due to changes in ALVEOLAR lung tissue
rather than the presence of mucus and inflammation in respiratory
bronchioles

Often co exist
 Case 2
62-year-old refinery engineer presents with progressive SOB
with copious yellow-green sputum. He denies hemoptysis,
night sweats, chills, and paroxysmal nocturnal dyspnea. He
has been treated for similar episodes of coughing and
shortness of breath during the past two years. He appears
tired and anxious. He appears blue with pitting edema of the
ankles.

Whats happening here?

 Chronic bronchitis
Persistent productive cough
for at-least 3 consecutive
mo. in at-least 2
consecutive years

( bloater
s)

Blue bloaters (type II respiratory failure)

- hypoxia drives respiration
- central cyanosis( hypoxia driven
vasoconstriction)
- low pO2, elevated pCO2 ( blue)
- sleep apnoea, cor pulmonale, respiratory
Copstead & Banasik
infections
Pathogenesis CIGARETTE SMOKE and POLLUTANTS

Chronic bronchitis chronic airway inflammation- NO EOSINOPHILS

loss of cilia &

Squamous metaplasia
smooth muscle hypertrophy
Airway fibrosis

Goblet cell hyperplasia

Increased bronchial wall HYPER SECRETION OF Microbial infection

thickness MUCUS

Tobacco effects
1.Trasncription of mucin gene
MUC5AC in bronchial airflow obstruction
epithelium FEV1, FVC
2.Production of neutrophil FEV1/FVC~ 25%
elastase
3.IL- 13 by T lymphocytes
Dyspnea hypoxemia and death

( Blue bloaters )
Morphology

Hyperaemic and swollen

mucosa of large airways
Mucus secretions
Reid index ( 0.8)
Normal thickness of
submucosal gland layer
to that of the bronchial
wall is 0.4 chronic
bronchitis
submucosal fibrosis
Coexisting emphysema
 Case 3
Mr PP 42yr old presented to his GP with increasing shortness
of breath after climbing stairs. He was given inhalers but
denies improvement. Now he presents to ED with SOB on
walking small distances within the home and unable to
complete sentences. He denies productive cough and chest
pain. He has no prior significant medical history and no
known allergies.

What more would you ask?

What would you look on examination?

What is the provisional diagnosis?
How do we investigate him?
Emphysema
Smokes 2 packs cigs
every day for 25yrs
No family history
Vitals: RR
Respiratory Examination:

Hyperventilating
Barrel chest (AP dia )
Poor chest expansion
Diminished breath sounds
(hyper inflated and air Weight
trapping) loss
Hyper resonant on percussion
Pink Puffers
Tactile vocal fremitus
 Investigations
FBC: PCV, WCC (s/o infection)
Pulse oxymetry: low PaO2, mild PaCO2 retention
ABG: to r/o resp. failure
PFT: Obstructive type
Sputum culture
X ray chest
ECG: RHF

Complications
Infective exacerbation
Bullous emphysema ---Pneumothorax
Respiratory failure ---Coma
Cor-pulmonale
 TTGFB gene
regulates
mesenchym
Reactive O2 spp =free al function
radicals ---inadequat
e repair of
elastin in
Pathogenesis

ECM

loss of
elastic recoil
causing
permanent
dilatation of
alveoli
WITHOUT
FIBROSIS

Elastin degradation
Defective
wound repair
 Most common

classification of emphysema
Smoking and coal
dust
Upper lobes
pale pink lungs

Alpha 1
Morphological

antitrypsin
deficiency
Lower lobes
Pale large lungs
Post
infection/atelectasis
Close to pleura
Upper lobes
Bullae
---Pneumothorax

Healed Infections
Old TB infection
Lung apices
Voluminous lungs
Increased compliance
Look for bullous blebs
MICROSCOPICALLY
Panacinar emphysema
Centriacinar emphysema
 Case 4
A 55 yr old male presents with fever,
severe persistent cough with foul
smelling sputum. At times he has
coughed frank blood. He was treated
recently with antibiotics for URTI .

What does the picture show ?

Whats happening here ?
 Bronchiectasis
Permanent dilatation of bronchi and bronchioles due to
destruction of muscle/elastic tissue along with chronic
necrotizing infection
A complication
Secondary to persisting obstruction and infection
Tumours, FB, COPD
Viscid mucus plugs : cystic fibrosis
Necrotising pneumonia
Kartagener syndrome
Immunodeficiency states
Clinical features
Fever
Severe persistent cough with expectoration of foul smelling
sputum
Blood streaked, frank hemoptysis
Weight loss, clubbing
Recent h/o URTI
 Bronchiecta
sis
Morphology
Lower lobes ( vertical) bilaterally
Irreversible dilatation of distal
bronchi and bronchioles ( 4 x the
usual diameter, can trace to the
pleura)
Acute and chronic inflammation
Peri-bronchial fibrosis

Complication
Lung abscess
Fungal ball
Brain abscess

Treatment
Postural drainage
Antibiotics
Bronchodilators
Surgical lobectomy rarely
 Summary of OLD

4 prototypes
Ultimate : airway obstruction ---- particularly during
expiration
More force is required to expel air (AWR)and emptying is slower ( FEF25-75)
Obstructive pattern : FEV1 / FVC ratio (FEV1, FVC unchanged)

Asthma is usually reversible and episodic

Chronic bronchitis is a clinical entity, affects
bronchi/oles
Emphysema is a morphological entity & destroys
acinus
Bronchiectasis is usually a complication
Can present as
Emergency ( status asthmaticus)
Exacerbation of COPD (Infections )
Thanks