COPD Flashcards
Clinically what does the patient presents with in chronic bronchitis?
Can’t get rid of carbon dioxide at the alveoli leading to increased PACO2 –> decreased PAO2 –> decreased PaO2 –> Hypoxaemia and hypercapnia
–> cyanosis of the skin + the mucus membranes
Call pulmonale
Respiratory acidosis
Dyspnoea, and spiritually wheeze, productive cough, tend to be fat, hypoxaemia
Histologically what do we see as a result of irreversible fibroses at the chronically inflamed segmental bronchi + bronchioles?
@ Segmental bronchitis CASH
D creased ciliated epithelium, acute inflammation leading to chronic inflammation, squeamish metaplasia, hypersecretion of mucus at the submucosa – trachea and Bronchi
@Bronchioles GMC
Goblet cell metaplasia, mucus plugs, chronic inflammation and fibrosis
What is emphysema?
It’s permanent enlargement of parts or all of the respiratory unit including the respiratory bronchioles the Alveolar ducts and the alveoli
Give two other types of emphysema ?
Paraseptal emphysema which is a localised disease at the subpleural location it targets the Alviola Dr love you
Causing the rupturing of M subpleural blabs leading to spontaneous pneumothorax . No obstructive airway disease
Irregular emphysema is a localised disease produces scar tissue. And no Obstructive airway disease
Clinically what does a patient with bronchiectasis present with?
Cough productive – cupfuls of sputum = foul-smelling due to sitting in the long and rotting
CO2 trapping leading to hypoxaemia leading to cor pulmonale
Haemoptysis
Digit clubbing
Deposit Amyloid – secondary amyloidosis
What is emphysema?
Permanent enlargement of all/part of the respiratory unit equals resp-bronchioles, Alveolar ducts, Alveoli
Where is the obstruction in emphysema ?
@Emphysema – >Decreased recoil – >decreased compliance – >lose radial traction = drag wall of bronchioles as Air accelerate out – > bronchioles Close/small airway collapse – > Small airway collapse usually @distal terminal bronchiole = prevent air escaping – > Distend respiratory units that have lost elastin behind collapsed bronchiole –>obstruction
What is emphysema an imbalance of?
Proteases and antiproteases
1.smoking = most common cause of emphysema
2.alpha-1 antitrypsin deficiency
1+2 – > (protease >antiprotease) – >Destroy alveolar Sac – >emphysema
When something gets down into the lung what defence mechanism Is present to prevent damage?
Something gets down by chance – >macrophage phagocytosis – >cause inflammation at the alveolar Air sac – > Makes proteases = damages the lung
Long makes antiproteases = alpha-1 antitrypsin which prevents proteases from damaging the lung
What are the types of emphysema?
Centriacinar>panacinar
Smoke hits central part of acinus
@ apical segment of upper lobe
Term + resp bronchioles
What are the clinical features of emphysema?
Increased AP diameter – >reset FRC
Pink puffer, Pursed lips = Respiratory alkalosis
Prolonged exploration – breathe slowly/require BARE effort – >Lose weight
Dyspnoea, non-productive cough,
RVH – Cor pulmonale
What is panacinar emphysema due to?
Alpha one antitrypsin deficiency
Alpha-1 antitrypsin counteracts elastase therefore prevents elastin from being broken down
Deficiency = Protein is made BUT not put in blood
Liver still makes protein – >mutation equals miss folded protein – >protein accumulates @ER of hepatocytes = pink PAS globules – >damage to hepatocytes – >cirrhosis
PiM/PiM = Normal PiM/PiZ = make half normal alpha anti trypsin PiZ/PiZ = VERY bad deffo get panacinar emphysema and cirrhosis
What is bronchiectasis ?
Abnormal/permanent dilation of the bronchioles and bronchi i.e. larger airways – >gets repeated opposite of airway infection and inflammation
How does the airway dilation lead to air trapping?
Airway dilation –> loss of tone –> air trapping
What is the effect of chronic necrotising inflammation On the Bronchi and bronchioles?
Destroycartilage + elastic – >dilate bronchi/bronchioles – >repeated episodes of airway infection + inflammation
