Providing in-depth revision notes for COPD pathophysiology. Including the causes, symptoms, triggers, risk factors, treatment and diagnosis. Excellent revision for exam period or also just to use a guide for your own revision. Originally made for pharmacy course, however can be used for any course ...
COPD
Cells trigger radicals
limitation that is usually
immune response.
progressive and associated with
Macrophages have a
an enhanced chronic
key role.
inflammatory response to
Chronic
noxious particles/gases in the
inflammation.
airways and the lungs.
Leads to irreparable
Problems with tissue damage.
breathing/shortness Development of
of breath COPD.
Classification: Oxidative Stress & COPD:
Mostly irreversible but Type A - Emphysema Cigarette smoke/environmental
can be alleviated with -Shortness of breath for few years. Type B - Chronic Obstructive triggers = increased oxidative stress
medication. -Absence or non-productive cough. Bronchitis and increased reactive oxygen species.
-Recent weight loss. -Progressive increase in SOB &
-Narrowed pulmonary vessels. activity.
-Barrel chest with flat diaphragm & over- -Chronic production cough for
many years. Thickening of
inflation of lungs.
Low O2 in outer wall
-Moderate hypoxaemia. -Gradually increase in severity &
blood
-Normal PaCO2. duration/limitation. Lungs will want to
Central space Free radicals which attack
-Excess distribution of ventilation to high protect themselves so
where air will lungs and damage
dead space areas they increase
Macrophages - Attack pass down epithelial surface of lungs
Proteases imbalance leads to inflammation and
breakdown alveoli walls - and destroy bacteria. immune response.
lungs lose their elasticity. Cilia brush away
dust, bacteria &
Inflammation of the Narrowed infections.
airways. bronchioles = Septum’s
Increased mucus Narrowed airways separate the
production. Acute Bronchitis - Inflammation walls of
-Enlargement of mucus of the large bronchi in the lungs alveoli.
secreting glands. that is usually caused by viruses Pathophysiology of Emphysema:
-Increased goblet cell Chronic Bronchitis - The presence
or bacteria and may last several Loss of elasticity
proliferation. of chronic bronchial secretions,
days or weeks. -Reduced a1-anti-trypsin,
-Inflammatory cell enough to cause expectoration, One large
occurring on most days for a resulting in destruction of elastic
proliferation. Mucus fibres. air sac
-Poor correlation to severity. minimum of 3 months of the
production Collapse of alveoli
year for 2 consent years.
-Loss of reticular structure.
-loss of associates vasculature.
Pathogenesis of Exacerbations: If you have COPD and have
Healthy COPD Increases airway inflammation and systemic additional infections, then
patient patient No more anti inflammatory effects. the inflammation in
protease so Most COPD exacerbations are triggered by respiratory lungs is increased.
Protease which COPD
Roflumilast - tissues get viral infections.
breaks down degraded. Treatment of COPD:
PDE4 inhibitor Respiratory viruses can be identified in the airway
tissue Bronchodilators
by PCR. aim up to 60% of exacerbations.
Alpha 1 Corticosteroids
Phosphodiesterase-4 antitrypsin - Virus associated exacerbations tend to have more
Oxygen therapy
airway and systemic inflammation.
stops protease Pollutants that reach the airways might also be
PDE4 Inhibition: B2 receptor agonist,
cAMP is a main trigger for many associated with precipitating exacerbations.
antimuscarinic agents,
cell signalling pathways. Airway bacteria are involved in causing
Breaks down cAMP from theophylline,
PDE4 is a major cyclic AMP exacerbations.
AMP.
metabolising enzyme expressed on cAMP is used for all Blocking
PDE4 helps Inhaled Corticosteroids: Adrenergic Receptors:
nearly all immune and pro- pathways causing
relieve COPD Glucocorticoids activate the a-adrenergic receptors
inflammatory cells. bronchodilation.
symptoms. glucocorticoid receptor. B-adrenergic receptors
Inhibition of PDE4 leads to Don’t want AMP to be Inhibits the inflammatory -B1 receptors are found mainly in the
increases cAMP levels in cells and formed - want cAMP. stimuli. heart, responsible for the effects of
reactivation of signalling
Effects many genes catecholamines.
pathways involved in reducing PD4 is the primary cAMP-
implicated in this process. -B2 receptors are responsible for causing
inflammation. hydrolysing enzyme in
Decreases inflammation. smooth muscle relaxation in many
inflammatory and immune
other tissues.
cells.
Trigger for
inflammatory Bronchodilators:
pathways Used in addition to SABAs/
LABAs.
Block effects of acetyl choline.
Ipratropium is a quaternary
derivative of atropine - does not
discriminate between muscarinic
Oral Mucolytics: receptor subtypes.
Carbocisteine and N-acetylcysteine are Inhibition of muscarinic GPCR
the oral mucolytics licensed for use in leads to muscle relaxation.
people with COPD.
Excessive mucus production in Salbutamol,
impairing airways. salmeterol,
NAC hydrolyses the disulphide binds of formoterol
mucus proteins.
Decreases mucus viscosity.
Facilitating mucus clearance.
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