Obstructive Disease – COPD

Question 0

What are the spirometry changes in COPD?

Answer 0

Decreased FEV1, D creased FVC

FTV one Decreases more than FVC
D creased FEV1: FVC ratio

Question 1

In COPD is there a problem with emptying or feeling?

Answer 1

Can’t empty – > air is trapped

Question 2

Define asthma.

Answer 2

An episodic + reversible bronchoconstrictive airway disease = extrinsic + intrinsic & targets the
bronchi +
Bronchi subdivisions +
Non-resp. bronchioles

Question 3

In the early phase reaction of asthma What’s mediators are produced and what are the effects?

Answer 3

Histamine:
bronchoconstriction,
dilate SM arterioles,
increased permeability @ post cap venules,
Produce nasal + bronchial mucus, Pruritus, Pain

LTc4d4e4+ PGD2:
Bronchoconstriction
Vasoconstriction
Increased permeability @ post cap Venues

PAF = leukocyte recruitment =
Monocyte, eosinophils, neutrophils

Question 4

What does the late phase reaction of asthma involve?

Answer 4

The mast cell releases eotaxin – >attracts + activates eosinophils – >releases major basic protein and cationics protein – >damages the epithelial cells + Airway construction

Question 5

In asthma what is the histology like in the bronchi and bronchioles?

Answer 5

@Broncho: 
Thick basement membrane, 
Hypertrophy of submucosal gland, smooth-muscle
Edema
Mixed inflammatory infiltrate

@bronchioles:

• Patchy loss of epithelial cells + goblet metaplasia
• Crystalline granules @eosinophils = breakdown @sputum– >Coalesce – >Charcot Leyden crystals
• Thick basement membrane
• Smooth-muscle hypertrophy and hyperplasia
• Spiral mucus plugs containing shed Curschmann spirals = Epithelial cells caused by MBP and cationic protein

Question 6

Clinically What is seen in asthma?

Answer 6

1. Eosinophilia
2. Episodic expiratory wheezing
3. Nocturnal cough
4. trapping + increased airway – >increased ant. post. Diameter

4.patient works hard to expel air through inflamed airways – > RESP alkalosis– >If bronchospasm not too relieved – >RESP acidosis – >intubate + mechanical ventilation– >
Severe asthma /Bronchoconstriction not relieved
–>status asthmaticus – >death

Question 7

What are the risk factors for intrinsic asthma?

Answer 7

Stress smoking exercise
Air pollutants = ozone
Virus
Aspirin = block COX – > no PG/Thx A2
\+
Leave LOX open for Leukotriene production

Aspirin induced asthma = Asthma + nasal polyps

Question 8

Explain chronic bronchitis/blue bloater ?

Answer 8

Smoking/CF – >mucus glands go through hypertrophy and hyperplasia therefore thickness of gland layer/Thickness of bronchial wall >50% = Reid index– >Hypersecretion are mucus at bronchus and subdivisions – >(productive cough for >3 months/year for >2 years) + (Mucus plugs at segmental bronchi + bronchioles – > airway obstruction = Irreversible fibrosis @chronically inflamed segmental bronchi +bronchioles

• Histology @segmental bronchitis: D creased cilia, acute’s inflammation ->chronic inflammation, squamous metaplasia, hypersecretion
• Histology at bronchioles: goblet cell metaplasia, mucus plugs, chronic inflammation

Question 9

Define emphysema?

Answer 9

Permanents/abnormal enlargement of all or part of the respiratory unit e.g. Bronchioles, Alviola ducts, alveoli

Question 10

In emphysema where is the obstruction?

Answer 10

There is no anatomic construction or mucus plugging
Obstruction = physiologic
Normally when you breathe – >alveoli feels with – >snapback = elastic recoil – >blow at out

@Emphysema destroy alveoli – >decreased elastic recoil – >increased compliance – >lose radial traction – >drag wall of bronchiole as Air accelerate out– >Bronchiole collapses – >Air trapped behind collapsed bronchiole usually @distal terminal bronchiole – >prevent air escape distal to collapsed airway – >distend parts of respiratory unit that have lost in elastin– >Obstruction

Question 11

What is emphysema an imbalance of?

Answer 11

Proteases e.g. elastin and auntie proteases e.g. alpha-1 antitrypsin

Question 12

Explain the relationship between proteases and anti-proteases in the alveoli when something gets down there ?

Answer 12

By chance something gets down – >macrophage phagocytosis – >causes inflammation at alveolar Air sack – >make proteases e.g. elastase = damage lung

Long makes antiproteases e.g. alpha-1 antitrypsin which counteracts proteases e.g. elastase

Question 13

What effect does smoking and alpha-1 antitrypsin deficiency have on proteases and antiproteases?

Answer 13

Smoking = most common cause of emphysema/alpha-1 antitrypsin deficiency – >
Protease >antiprotease – >destroy Alviolar air sac – >emphysema

Question 14

What is the most common type of emphysema?

Answer 14

Centriacinar >pan acinar

Question 15

Explain centriacinar emphysema?

Answer 15

Smoke enters and hits central part of acinus = centri acinar emphysema

Usually at apical segments of the Upper lobe – Terminal bronchials, respiratory bronchioles

Question 16

Define panacinar emphysema ?

Answer 16

Due to alpha-1 antitrypsin deficiency

Elastic breaks down elastin into broken down elastin
Alpha-1 antitrypsin counteracts elastase

The deficiency is that the protein is not put inside the blood
Liver makes protein – >it is mutated/miss folded – >protein accumulates at ER of hepatocytes = pink PAS globules – >Damage hepatocytes – >cirrhosis

Question 17

Explained mutation of panacinar emphysema in terms of the genes.

Answer 17

Normal allele = PiM/PiM

If PiM/PiZ: = Usually asymptomatic + produce only half the normal amount
PiM/PiZ -> smoke -> emphysema

If PiZ/PiZ -> increased risk of pan acini emphysema + liver cirrhosis

Question 18

What do we see clinically and emphysema?

Answer 18

Pink puffer pursed lips prolonged exploration
Increased AP diameter – barrell chest
 dyspnoea
Non-productive cough 
Core pulmonale

@Emphysema – >lose elastic recoil – >increased compliance – > (Chestwall expand Out >collapse in) -> increased AP diameter – barrel chest, + reset increased FRC

Question 19

Explain how emphysema leads to cor pulmonale

Answer 19

Prolonged exploration – >destroy Alviolar airsac – >lose recoil + lose capillaries @wall of air sac -> lose oxygen exchange bed – >Hypoxaemia PaO2 < 60 -> vasoconstriction = pulmonary hypertension – >RVH – >RHF = cor pulmonale

Question 20

Explain bronchiectasis?

Answer 20

Abnormal/permanent in lodgement of the bronchi (+ bronchioles) larger airways– >Repeat episodes of airway infection and inflammation

Question 21

Explain how airway dilation leads to air trapping

Answer 21

Airway dilation – >loss of tone – >air trapping

Question 22

Explained the pathophysiology of bronchiectasis

Answer 22

Chronic necrotising inflammation – >destroys cartilage and elastin – >permanent enlargement of bronchitis/bronchials – >repeated episodes of the airway infection and inflammation

@CF – >Sick sick creations – >mucus plugging – >increased infection risk – >bronchiectasis

@Tumour/foreign body inhale – >block – >increased risk of infection – >bronchiectasis

@Allergic bronchopulmonary aspergillosis: asthma/CF – >aspergillus HSR – >damage airway – >bronchiectasis

@Necrotising infection (TB S aureus H. influenzae Adenovirus, MAI– >Bronchiectasis)

@Kartagener syndrome/primary ciliary dyskinesia

Question 23

What do you see clinically with bronchiectasis ?

Answer 23

Secondary amyloid disposition, digit clubbing, productive cough - cups of mucus Smell horrible due to sitting in lung and rotting
Haemoptysis, CO2 trapping – >hypoxaemia – >cor pulmonale