COPD Flashcards
(20 cards)
- COPD is a — and — disease with some significant — effects that may contribute to
the severity in individual patients - Its pulmonary component is characterised by — that is not —
- The airflow limitation is usually — and associated with an abnormal — response of
the lung to — particles or —
preventable and treatable
extra pulmonary effects
airflow limitation
fully reversible
progressive
abnormal inflammation
noxious particles or gasses
- FEV1 is the amount of — you can – out of your lungs in —
- FVC is the — of air that can be — during a—
definitions: - COPD is a lung disease characterised b —
(FEV1/FVC ratio of less than —%) that is not — - COPD comprises of 2 predominant conditions — and —
- Chronic bronchitis is defined as a— for — in each of – successive years in a patient whom other causes of — has been excluded
- Chronic bronchitis is a disease of — blocking airways
- Emphysema is defined as the presence of — of airspaces — to the —- or — with — of their walls without obvious —
- Emphysema is a disease of loss of — around acini and terminal bronchioles
air
force
one second
total volume
exhaled
max expiration effort
airflow limitation
70%
not fully reversible
chronic bronchitis and emphysema
productive cough
3 months
2
chronic sputum
mucus blocking
enlargement
distal
terminal bronchioles or acinus
destruction
fibroids
elastic tissue
incidence:
* COPD affects >10% of the population of the USA; 200
million people worldwide
* Objective evidence of — and —- airflow obstruction
* Affects 14% of male smokers versus 3% of non-smokers
(i.e. smoking is not the only cause of COPD!)
* COPD is the fourth leading cause of death in western
world
* The only common cause of death increasing in incidence
aetiology:
* 90% of cases occur in —
* 25% of heavy smokers have —
* — : high risk
* Environment: — >—
▪ Air pollutants including sulphur dioxide, nitrogen
dioxide
* Dusty occupations (coal, quartz, silica, welding)
* Passive smoking
* Low birth weight; chest infections in the first year of life
(e.g. — )
persisting and irreversible
chronic smokers
chronic bronchitis
age
urban > rural
adenovirus
chronic bronchitis:
* — and production of — on most days for a period of at least — months in at least — consecutive years
* Common among — and —
* Defining feature of — hypersecretion is primarily a
reflection of — involvement
* Airflow — component is due to —– involvement
with:
▪ Inflammation, fibrosis and resultant —- of bronchioles
(small airway disease)
▪ Co-existent —
productive cough
sputum
3
2
cigarette smokers and urban dwellers
mucus hyper secretion
bronchial involvement
obstruction
peripheral involvement ]
narrowing
emphysema
pathogenesis of chronic bronchitis:
* Hypersecretion of — , beginning in the — airways
* — induce hypersecretion of the bronchial mucus glands
-> — of mucus glands -> —- formation of mucin secreting — cells in surface epithelium
* Irritants also induce inflammation with — , — and —
* Gross appearance: Airways — and — , covered by a layer of mucin / mucopurulent secretions
* Histologically:
▪ — of mucus secreting glands
▪ Increase in number of — in the lining epithelium
▪ Loss of — cells
▪ Inflammatory cell —
▪ May eventually lead to — -> — -> — cell —
mucus
large
irritants
hypertrophy
metastatic formation
goblet cells
cd8+ t lymphocyte , macrophages , and neutrophils;s
swollen and ertheymouatous
hypertrophy
goblet cells
ciliated epithelial cells
infiltrate
squamous metaplasia –> dysplasia —> squamous cell carcinoma
hallmark of chronic bronchitis:
* Mucus gland —
* Increase in —
* Loss of —
* May get —
clinical course:
* — with production of — may persist without —
* May progress to significant — with airflow — -> — , — and —
* Severe forms may develop — and –
* Recurrent — and —
hypertrophy
goblet cells
ciliated cells
squamous metaplasia
cough
sputum
ventilatory dysfunction
COPD
airflow obstruction
hypercapnia, hypoxaemia and cyanosis
pulmonary hypertension and cardiac failure
infection and respiratory failure
emphysema:
* — — of air spaces — to the
—- accompanied by — of their
walls
* (Morphologic definition)
epidemiology:
* — > —
* —
* Develops over many years becoming clinically significant
in later life
* Anatomically, emphysema involves the – , a structure — to the —
* This — portion of lung is lost in emphysema
permanent enlargement
distal
terminal brochioles
destruction
male > females
heavy smokers
acinus
distal to terminal bornchioles
air exchanging
1- respiratory acinus:
* Portion of lung tissue formed by the — of a single —
* Includes — , —, —
* Fundamental unit of –
2- lung lobule:
* — area of lung parenchyma — cm across outlined by —
* Contains lung tissue supplied by — , —
* Consists of – , —
* Grossly —
branching
terminal bronchioles
bronchiole m alveolar duct , alveoli
lung
hexagonal
1-2
fibrous septa
3-5 terminal bronchioles
3-5 respiratory acni
visible
TYPES OF EMPHYSEMA:
* Defined according to the distribution in the — and —
1- Centriacinar:
* — or — part of — affected; sparing of —
* More common and severe in — lobes
2- Panacinar
* Acini are — — from the level of the — to the —
* More commonly affects — zones
3- Distal acinar
* Predominantly affects the — part of the —
* Most — adjacent to he —
* Most often associated with —
lobule and acinus
central or proximal of acini
distal alveoli
upper lobes
uniformly enlarged
terminal bronchiole to terminal blind alveoli
lower zones
distal part of acinus
striking
pleaura
penumothroax
more info:
C e n t r i a c i n a r
- b o t h e m p h y s e m a t o u s a n d
normal airspaces exist within t h e
s a m e a c i n u s .
- m o r e c o m m o n a n d s e v e r e i n t h e
upper lobes, particularly in the
apical segments.
- m o s t c o m m o n l y s e e n a s a
consequence o f cigarette
smoking
P a n a c i n a r
- acini a r e uniformly enlarged from
t h e l e v e l o f t h e r e s p i r a t o r y
b r o n c h i o l e t o t h e t e r m i n a l b l i n d
alveoli.
- m o r e commonly i n t h e lower lung
- occurs in a
pathogenesis of emphysema:
* At — level the airflow suddenly — , dropping particulates into adjacent —
* — and — elastases are turned on by
particulate or other compounds of smoke
* —- is secondary to elastase and —
terminal bronchiole
decreases
alveoli
neutrophils and macrophages
septal destruction
protease activity
1- imbalance between proteases and antiporteases in lung:
* elastase is one of many proteases present in — and —
* Elastases are released during the — process
* Antiproteases such as Alpha 1 Antitrypsin (A1AT) counteract their effects
* Patients with hereditary deficiency of A1AT have a high incidence of –
2- neutrophils in lungs:
* They are normally — in the lung
* Any stimulus that increases their number or the release of their —-containing granules increases — activity
* Macrophages also a significant source
* Both sources play a role in — related emphysema
- info:
* — and imperfect — are central in the pathogenesis of emphysema
macrophages and neutrophils
inflammatory process
emphysema
sequestered
elastase containing
elastolytic activity
smoking
elastin degradation
repair
1- bullous emphysema:
* Form of emphysema with — spaces or — (> – cm)
* Most often subpleural near the — →—-
2- ALPHA 1 ANTITRYPSIN DEFICIENCY:
* A1AT is a —-
* It inhibits — elastase
* A1AT deficiency common in European population
* — normal alleles —
* Abnormal allele —
* Patients develop — onset COPD with — lobe
emphysema, bronchioestasis worsened by —
large subpleaural or bullae
>1 cm
apex repture –> pneumothroax
serine protease inhibitor
serine protease inhibitor
neutrophils
autosomal recessive
PiMM
PiZZ
early
lower
smoking
clinical correlation:
* Many patients with pure emphysema develop — and — due to loss of — delivery to the —
* — with slow forced —
* Combined with chronic bronchitis may have associated — heart failure — BLOATER
* — of Emphysema is more important than the —
* As it becomes more severe it becomes difficult to —
* Pink Puffer and Blue Bloater represent opposite ends of
the spectrum of Emphysema and Chronic Bronchitis
progressive dysponea and weight loss
02 delivery to periphery
pink buffer
slowed expiration
right hf blue bloaters
severity
type
classify
Chronic Bronchitis
* 40-45 onset
* — , — dyspnoea
* Sputum —
* Infections —
* —
* — elastic recoil
* CXR: –
* —
Emphysema:
* 50-75 onset
* — — dyspnoea
* — sputum
* Infections —
* Cor pulmonale rare
* — elastic recoil
* — , – heart
* –
mild late
abundant
common
cor pulomale
normal
cardiomegaly
blue bloater
early severe
scant
uncommon
low
hyperinflation , small heart
pink buffer
clinical presentation:
* SOB, wheeze
* — cough
* Recurrent chest infections
* — chest pain
* Features of – heart failure
* Narrowed airways lead to — of lungs which are unable to empty
* This leads to exertional dyspnoea, and progresses to
dyspnoea at rest
disease course:
* Asymptomatic early on until FEV1< —
* Hyperinflation at rest and worsens with exercise
* Muscles of respiration have increased work due to
increase functional residual capacity
* On examination:
▪ Use of accessory muscles of respiration
▪ Pursed lip breathing
▪ Hyperinflation
▪ Decreased breath sounds on auscultation; — , —
▪ Features of right heart failure
* Diffusing capacity decreases
productive
pleaurtic
right
hyperinflation
<50
wheeze , rhonchi
gold initiative:
* International Workshop established 1998
* Staging system for COPD
* Mild to Severe Stage 1-4
* — is the gold standard for diagnosis and assessment of COPD
* FEV1/ FVC ratio < — % indicates airflow limitation
prevelance of stages :
* Stage 1 - prevalence 2.5%
* Stage 2-3 - prevalence 1.1%
* COPD diagnosed in 5th and 6th decades
* Probably starts much earlier
spirometry
<70
COPD mortality:
* PROBABLY —
* Identifying precise cause of death in elderly patients is
difficult
* Patients may have cardiac arrhythmias, ischaemic heart
disease, pulmonary emboli etc.
Death in COPD
Due to:
1. Respiratory — and —
2. Cor pulmonale = — -sided heart failure due to chronic —
3. Massive — of lungs secondary to —
underestimated
resp acidosis and coma
right sides due to chronic pulmonary hypertension
massive collapse 2dary to pneumothorax
air flow restriction:
* The issue of air flow restriction and air way trapping,
due to a loss of — , can be a little confusing
* The cause of air trapping: when you breath in the chest— , when you breath out the chest
—, pressure in the alveolus — causing a pressure gradient between the — and the — , air flows through the —
elastic tissue
expand
contracts
increases
alveolus and airway
small bronchioles
air way restriction principles:
1. Bernoulli’s principle:
* This states in fluid dynamics where there is an — in the speed of a fluid across the constriction, this is associated with a — in pressure (aircraft wings and sails).
* This means that if there is a constriction with fluid flow, the pressure — , causing the — to further tighten.
2. Poiseuille’s Law
* The velocity of a fluid through a narrow tube varies with the forth power power of the radius of
the tube. The resistance to flow is inverse of
radius to the power of 4.
* In another words, tiny variations in radius of a
tube has a huge effect on the — to flow.
increase
decrease
decreases
constriction
obstruction
AIR FLOW RESTRICTION PRINCIPLES
(CONTINUED)
* When you breath out the chest — , air flows through the — , which act as a — point
the pressure in these drops as the air flow — , the
pressure drops across the “constriction” and there is a
tendency for the of the bronchioles to constrict further
because of this
* Normally elastic tissue holds them open. If you have lost
your elastic due to COPD, or other problems, the
bronchioles — . Any tiny variations in constriction
has a huge effect on the air flow limitation
* The air flow stops - air trapping
* Elastic tissue opposes Bernoulli’s principle
contracts
small bronchioles
consitrciton point
increass
constricts
