Resp Patho Flashcards
Describe the airways -r espiratory tree and the order of contents from trachea to alveolus
- Lack of cartilage from terminal bronchiole- more distensible but vulnerable to comrpession
- Hierarchial branching
- Alvoli - exchanger unit
- Before alveoli - conduits/thoroughare
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How does the airway reisstance change in the repsiratory tree?
- Airway reisstance is macimum at 5th-8th gen broncho
- It falls beyond 10th gen
- As increased cross section over-compemnsates for the progressive narrowing.
Lung Parenchyma - describe
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WHat are the Laws of Gas Exchange
- Can only occur in the alveolus
- That is both ventilated and perfused
- Alveolocapillary membrane is key
Ineffeciencies in gas exchange
- Ventilation of non-perfused alveoli- DEAD SPACE
- Perfused unventilated alveoli- R2LS– right to left shunt- entry of deoxygenated blood from pulmonary to systemic circulation
- So, the entire conduit from nose and up to but excluding the alveoli- ANATOMICAL DEAD SPACE
- R2L Shunt- is generally not physiological/anatomical, almost always pathological
- These cause ventilation perfusion V/Q mismatch
hysiological inefficiences in VQ
- Normal ratio 0.8
- But not uniform
- Base <0.8- better ventilated and perfused than apex
- Base better perfused than ventilated
- Gas exchange is also relatively inefficient but that is normal physiology
Functions of the lung
- Narrower than the functions of the respiratory system, as a whole, which also offers
- Speech and olfaction, humidification and temperature control, respiratory defence- gag, sneeze and cough
- Lungs- oxygenation, removal of waste gases e.g., CO2
Repiratory Failure - definitiona nd physiology
- Impaired ventilation - neuromuscular defect
- Impaired perfusion - vascular defect
- Impaired diffusion- intrinsic lung alveolar efect
- RF is defined as a condition in which there is failure in one or both of the gasexchange function of lungs
- Only O2 exchange- RF type I
- Both O2 and CO2- RF Type II
- Additionally type III- to be discussed and
- Type IV- hypoperfusion of respiratory muscles in shock patients
Impaired ventilation - causes
- Neural- Narcotics, Motor neurone disease (MND), Encephalitis, Cerebral space occupying lesion (SOL) etc
- Mechanical- obstruction to airways, kyphoscoliosis, pleural effusion, trauma, muscle disease, gross obesity (Pickwickian syndrome)
Why might you get impaired perfusion?
•Cardiovascular- heart failure, multiple pulmonary emboli
What are the Types of Respiratory Failure
- Type I- Hypoxia but low CO2 (hypocapnia), as hyperventilatory drive is retained but insufficient for delivery of adequate O2 to the exchange unit
- Type II- Hypoxia and hypercapnia- lack of ventilatory drive- hypoventilation
- Acute type II RF- Respiratory acidosis
- Chronic type II RF- Compensatory metabolic alkalosis
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What is the
Physical signs of repsiratory failure
- Dyspnoea
- Somnolence
- Headache
- Confusion
- Coma
- Asterixis (flapping tremor/hepatic flap)
VQ Mismatch (ventilation/perfusion mismatch).
- A hyperventilating normal alveolar unit cannot compensate for the hypoxaemiadue to shunt- anatomical or physiological (diversion from pathological dead space)- as the O2 loading graph plateaus off
- But it can compensate for the hypercapnia- as the CO2 unloading graph does not saturate and is linear
What are the adaptions in VQ Mismatch
- If V falls- PAO2 reduces causing pulmonary vasoconstriction and vascular diversion to healthy segment
- If Q falls- PaCO2 reduces causing bronchoconstriction and diverting air to healthy segment
- FIRST IN LAST OUT PRINCIPLE- Air from inefficient alveoli stays in dead space and then enters efficient alveoli in the next breath (physiological redistribution of air)
chronic osntructive airway disease - what is it
- Chronic bronchitis and Emphysema
- Depending on the level of involvement of the airway
- Distinct pathological processes
- Almost always a degree of overlap
- By definition, diffuse and generally irreversible or fixed
- Centred on smaller airways and alveolar units
- Local obstruction is by tumour or foreign body
It was once known as chronic obstructive airways disease (COAD). These days it’s called chronic obstructive pulmonary disease, or COPD. Both are the official medical names for chronic bronchitis and emphysema.
COLD (chronic obstructive lung disease): Any disorder that persistently obstructs bronchial airflow. COLD mainly involves two related diseases – chronic bronchitis and emphysema. Both bronchitis and emphysema cause chronic obstruction of air flowing through the airways of the lungs
Pathology of chronic bronchitis
- Chronic inflammation of airways, may have squamous metaplasia (smokers) or acute inflammation due to acute exacerbation even with bronchopneumonia (infective exacerbation)
- Bronchial associated lymphoid tissue or BALT
- Hyperplasia of goblet cells leading to mucus secretion, plugging and obstruction
- Hyperplasia of submucosal glands in larger airways
- Respiratory bronchiolitis- quintessential smoker’s lesion
Complications of chronic bronchitis
- Acute exacerbation
- Bronchopneuminia
- Bronchiectasis- permanent dilation of the bronchioles
Causes/ RFs of chronic bronchitis
- Smoking- causes inflammation due to oxidative injury- chronic bronchitis and emphysema
- Cystic fibrosis- emphysema
- Bronchial asthma- COPD overlap (out of scope for today’s lecture)
CLinicl presentaitona nd definition of chronci bronchitis
- Cough and sputum for 3 months in 2 consecutive years
- Almost always smokers
- Advice on smoking cessation therapy
- COAD changes not necessarily always reversible as an endogenous autoantigen unmasking theory has been recently proposed
EMphysema - what is this
- Abnormal enlargement or dilation of the alveolar air space distal to the terminal bronchiole
- Smokers with chronic bronchitis
- Emphysema
- Endogenous lipoid obstructive pneumonia is not a feature of COAD but seen in localized obstruction due to tumour and is rich in foam cells and plasma cells