[go: up one dir, main page]

0% found this document useful (0 votes)
117 views5 pages

241 - Respiratory Pathology) COPD - Pathophysiology

This document provides an overview of COPD pathophysiology. It discusses the risk factors, characteristics, and mechanisms of both chronic bronchitis and emphysema. Chronic bronchitis involves excessive mucus production leading to airway obstruction. Emphysema involves breakdown of lung tissue by proteases like elastase, destroying elastic fibers and causing airway dilation and reduced lung recoil. Both can cause hypoxemia and hypercapnia due to impaired gas exchange, though this occurs later in emphysema. Smoking is the primary risk factor for COPD development by damaging cilia, inducing inflammation, and impairing mucus clearance.

Uploaded by

youssef magdy
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
0% found this document useful (0 votes)
117 views5 pages

241 - Respiratory Pathology) COPD - Pathophysiology

This document provides an overview of COPD pathophysiology. It discusses the risk factors, characteristics, and mechanisms of both chronic bronchitis and emphysema. Chronic bronchitis involves excessive mucus production leading to airway obstruction. Emphysema involves breakdown of lung tissue by proteases like elastase, destroying elastic fibers and causing airway dilation and reduced lung recoil. Both can cause hypoxemia and hypercapnia due to impaired gas exchange, though this occurs later in emphysema. Smoking is the primary risk factor for COPD development by damaging cilia, inducing inflammation, and impairing mucus clearance.

Uploaded by

youssef magdy
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
You are on page 1/ 5

Last edited: 9/10/2021

1. COPD PATHOPHYSIOLOGY
COPD Pathophysiology Medical Editor: Dr. Sofia Suhada M. Uzir

Hypertrophy
OUTLINE
o Increase in the size of mucin glands
I) INTRODUCTION TO COPD Hyperplasia
II) RISK FACTORS ASSOCIATED WITH OF COPD o Increase in the quantity
III) CHRONIC BRONCHITIS
IV) EMPHYSEMA (2) Ciliary dysfunction
V) COR PULMONALE
Smoking causes extreme irritation
VI) REVIEW QUESTIONS
o This leads to destruction of cilia → ciliary shortening
VII) REFERENCES
and dysmotility → less efficient in beating the mucus
upwards → mucus accumulates in the airways
→ obstruct and narrow

I) INTRODUCTION TO COPD
Diseases categorized as COPD
o Chronic bronchitis
 Classically seen with mucus production
→ productive cough
 Usually diagnose clinically
• How much mucus produced
• How often
• How long Figure 1. Ciliary destruction cause mucus accumulation
o Emphysema
 Structural changes (3) Air trapping

COPD is not always clear cut, they often coexist When trying to exhale, bronchioles get a little smaller
o Elastin keeps them open
II) RISK FACTORS ASSOCIATED WITH OF COPD Mucus plug cause
Smoking o Narrowing the airway → the airway gets even smaller
o The main cause of COPD → a lot of air builds up, especially CO2
o Limit the amount of air going into the lungs (oxygen)
Environmental exposure o Limit the amount of air able to expire (CO2)
o Dust  More prominent than the inhalation
o Silica
o Air pollutes
Genetic condition
o Alpha 1 antitrypsin deficiency
 Least common
 Autosomal dominant
 Positive family history
 Underlying liver disease
 < 45-50 years old

III) CHRONIC BRONCHITIS


It is mucus related
Figure 2. Mucus plug causes narrowing of the airway, leading
(A) QUICK ANATOMY OF THE LUNGS to air trapping
Mucosal lining (4) Hypoxemia and hypercapnia
o Epithelial tissue with lamina propria
Hypercapnia
Submucosa o High partial pressure CO2
o Loose connective tissue with submucosal glands
Hypoxemia
Submucous glands naturally produce mucus o Low partial pressure oxygen
o To humidify the airways + keep the airways moist
o To trap certain types of pathogens Low oxygen coming in due to the mucous plug cause
o Significantly more CO2 building up especially during
(B) COMMON FINDINGS expiration
o CO2 start to build up in the blood → less oxygen
(1) Hypertrophy and hyperplasia of mucosal glands
makes it down the airway to perfuse into tissue
and goblet cells
 This cause V/Q mismatch → hypoxemia and
In chronic bronchitis, irritant causes agitation of the hypercapnia
mucosa → hypertrophy and hyperplasia of mucosal
glands → increase the alkaline mucous production
significantly to coat the area
o This leads to mucous plugging → narrowing and
obstructing the airways

COPD Pathophysiology RESPIRATORY PATHOLOGY: Note #1. 1 of 5


(5) Pneumonia (2) Alpha 1 antitrypsin
Increase risk of developing pneumonia due to mucus plug Liver release alpha 1 antitrypsin, which is an anti-
o Bronchopneumonia protease into the blood
 Diffuse scattering especially at the base of the They act by inhibiting the action of elastases
lungs o Breakdown the elastases and prevent it from
o Lobar pneumonia damaging the elastic tissue
 Consolidation In autosomal dominant (two defective copies) → deficient
in alpha 1 antitrypsin
o The liver cannot produce or produce very limited
amount of alpha 1 anti trypsin
o There is no inhibition of elastases → a lot of
elastases → damage to the elastic tissue occurs

(B) COMMON FINDINGS


(1) Air trapping
Figure 3. Lobar pneumonia vs bronchopneumonia
Limited recoil during expiration and collapse of airway
causes build-up of air inside the lungs
Bacterial infection responsible:
o Hemophilus influenzas (2) Dilation/expansion of small airway (the acinus)
o Moraxella catarrhalis Air trapped overtime cause → the small airways to
expand
IV) EMPHYSEMA
(3) Affections of the alveoli which may lead to
It is structural related
pneumothorax
(A) PATHOPHYSIOLOGY Elastic tissue is also loss in the alveoli → elastase
Alveolar macrophages → phagocytose pollutants → breakdown alveolar septa. This leads to:
macrophages become activated and release cytokines o Loss in alveoli that increase surface area
o Cytokines activate neutrophils and more o Balloon out area of acinus → can cause
macrophages to be recruited to the area pneumothorax
o Inflammation causes neutrophils and macrophages to
(4) Hypoxemia and hypercapnia
release proteases enzymes → elastase
o Elastases → breaks down elastin, which is the Happens in later stages in emphysema
connective tissue found in the lungs Inhalation of oxygen is subnormal → airway collapse
leads to CO2 build up → very mild hypoxemia and
(1) Functions of elastin hypercapnia
Chronic emphysema can develop severe hypoxemia
(i) Increase the lung recoil
and hypercapnia → which may lead to right sided heart
Increase in compliance failure as its complication
o Loss of elastin causes → easy expansion during
inhalation, but limited recoil to push air out during
expiration → air trapping Remember:
Remember: In emphysema
Inspiration o Air is able to enter the lungs during inhalation
o Requires respiratory muscles o Unlike chronic bronchitis, hypercapnia and hypoxemia
 Diaphragm happen at a later stage
 Intercostal muscles o During expiration, the airways get narrower due to the
o It helps in expanding energy → active process loss of elastic tissues → the airways collapse

Expiration is a passive process In chronic bronchitis


o When lungs reach the maximum capacity of inhalation o The airways get narrower due to the excessive mucus
→ elastic tissue draws the lungs back to the normal secretion
size

(C) TYPES OF EMPHYSEMA


(ii) Keeps airway open (1) Centriacinar Emphysema
Exhaling causes the airway to become smaller → elastic Pockets of air with decreased surface area in the
tissue pulls in the opposite direction → outward force → proximal airways → upper lobes of the lung
keeps the airway open
o Loss of elastic tissue leads to loss in the opposing (2) Panacinar emphysema
force → pressure inside the airway becomes very Decreased surface area affecting the distal airways
low → airway collapse → more airway trapping → lower lobes of the lung
Bernoulli principle: (3) Distal acinar emphysema/paraseptal
In the airway, there’s low pressure due to high velocity
airflow Affection of the distal alveoli in the peripheries of the
lung
This is near the visceral and parietal pleura area
o Affection may lead to rupture and form secondary
spontaneous pneumothorax (air in the pleural
space) → lead to compression atelectasis →
collapse of lungs

Figure 4. The Bernoulli principle of the airway


2 of 5 RESPIRATORY PATHOLOGY: Note #1. COPD Pathophysiology
(C) INVESTIGATIONS
Investigations that may be done to rule out right sided
heart failure include
(1) Brain natriuretic peptide (BNP) levels
made by the ventricles
(2) Echocardiography
To determine the decrease in ejection fraction
(3) Swan-Ganz catheterization
Gold standard
Right ventricular catheterization → check pulmonary
capillary wedge pressure (see if it is > 18 mm Hg)

Figure 5. Types of emphysema

V) COR PULMONALE
It is the complication that may happen in chronic
obstructive pulmonary diseases
o More common in chronic bronchitis or later stage of
emphysema

(A) PATHOPHYSIOLOGY
(1) Hypoxemic vasoconstriction
Normal autoregulatory mechanism of the lung
Normal V/Q =0.8
o In order to maintain this, decrease in ventilation
→ decrease in perfusion
In COPD, vasoconstrictions happen in multiple part of the
lungs
o Eventually pulmonary vessel will develop high
pressure
o Pulmonary hypertension
(2) Increase in workload
To push against the high pressure
o Right ventricle will have to increase its workload → to
maintain the same stroke volume
o This leads to right ventricular hypertrophy
→ overtime will cause failure

Figure 6. Summary of pathophysiology of cor pulmonale

(B) SIGNS OF RIGHT SIDES HEART FAILURE


Blood backs up into the superior and inferior vena cava
causing
o Increase jugular venous pressure
o Hepatomegaly/splenomegaly
o Peripheral edema

COPD Pathophysiology RESPIRATORY PATHOLOGY: Note #1. 3 of 5


VI) REVIEW QUESTIONS VII) REFERENCES
● Sabatine MS. Pocket Medicine: the Massachusetts General
1) The following diseases is included in the umbrella
Hospital Handbook of Internal Medicine. Philadelphia: Wolters
term COPD except Kluwer; 2020
a) Emphysema ● Le T. First Aid for the USMLE Step 1 2020. 30th anniversary
b) Chronic bronchitis edition: McGraw Hill; 2020.
● Williams DA. Pance Prep Pearls. Middletown, DE: Kindle Direct
c) Asthma Publishing Platform; 2020.
d) None of the above ● Papadakis MA, McPhee SJ, Rabow MW. Current Medical
Diagnosis &amp; Treatment 2018.
2) Long term exposure to which of the following can ● New York: McGraw-Hill Education; 2017.
increase the risk of COPD? ● Jameson JL, Fauci AS, Kasper DL, Hauser SL, Longo DL,
a) Airborne chemicals Loscalzo J. Harrison's Principles of Internal Medicine, Twentieth
Edition (Vol.1 & Vol.2). McGraw-Hill Education / Medical; 2018
b) Pollutants ● Marieb EN, Hoehn K. Anatomy & Physiology. Hoboken, NJ:
c) Lung irritants Pearson; 2020. Boron WF, Boulpaep EL. Medical Physiology.;
d) All of the above 2017.

3) Breathlessness/short of breath is called


a) Asthma
b) Bronchitis
c) Dyspnea
d) Winded
4) Chronic bronchitis may cause
a) Narrowing of the airways due to structural changes
b) Increase in mucus production
c) Hypertrophy of the epithelial cells
d) Air trapping due to destruction of the collapse of the
airways
5) In emphysema
a) Centriacinar emphysema affect the upper lobes
b) Distal acinar emphysema can lead to collapse of the
lungs
c) Panacinar emphysema causes the airway collapse
in the lower lobes
d) All of the following
6) Regarding cor pulmonale, which is true?
a) It happens early in emphysema
b) It is more common in chronic bronchitis
c) Vasodilatation plays a role in its pathophysiology
d) It happens due to the increase in the workload of the
heart and lungs
7) Which of the following is the gold standard for ruling
out right sided heart failure?
a) BNP levels
b) Echocardiography
c) Swan-Ganz catheterization
d) CT scan of chest
8) In chronic bronchitis, which is false?
a) It causes air trapping
b) May lead to hypercapnia
c) Caused by the destruction of the elastin fibers
d) There is hyperplasia of goblet cells
9) The most common cause of COPD is
a) Bronchiectasis
b) Smoking
c) Asthma
d) Emphysema

10) In right sided heart failure


a) There is increase in jugular venous pressure
b) Peripheral edema never occurs
c) There is never hepatomegaly
d) Splenomegaly always present

CHECK YOUR ANSWERS

4 of 5 RESPIRATORY PATHOLOGY: Note #1. COPD Pathophysiology


COPD Pathophysiology RESPIRATORY PATHOLOGY: Note #1. 5 of 5

You might also like