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U17 + 18 > Resp Patho > Flashcards

Resp Patho Flashcards

1
Q

Describe the airways -r espiratory tree and the order of contents from trachea to alveolus

A
  • 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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2
Q
A
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3
Q

How does the airway reisstance change in the repsiratory tree?

A
  • Airway reisstance is macimum at 5th-8th gen broncho
  • It falls beyond 10th gen
  • As increased cross section over-compemnsates for the progressive narrowing.
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4
Q

Lung Parenchyma - describe

A
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5
Q

WHat are the Laws of Gas Exchange

A
  • Can only occur in the alveolus
  • That is both ventilated and perfused
  • Alveolocapillary membrane is key
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6
Q

Ineffeciencies in gas exchange

A
  • 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
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7
Q

hysiological inefficiences in VQ

A
  • 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
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8
Q

Functions of the lung

A
  • 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
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9
Q

Repiratory Failure - definitiona nd physiology

A
  • 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
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10
Q

Impaired ventilation - causes

A
  • 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)
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11
Q

Why might you get impaired perfusion?

A

•Cardiovascular- heart failure, multiple pulmonary emboli

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12
Q

What are the Types of Respiratory Failure

A
  • 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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13
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14
Q

What is the

A
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15
Q
A
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16
Q

Physical signs of repsiratory failure

A
  • Dyspnoea
  • Somnolence
  • Headache
  • Confusion
  • Coma
  • Asterixis (flapping tremor/hepatic flap)
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17
Q

VQ Mismatch (ventilation/perfusion mismatch).

A
  • 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
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18
Q

What are the adaptions in VQ Mismatch

A
  • 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)
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19
Q

chronic osntructive airway disease - what is it

A
  • 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

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20
Q

Pathology of chronic bronchitis

A
  • 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
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21
Q

Complications of chronic bronchitis

A
  • Acute exacerbation
  • Bronchopneuminia
  • Bronchiectasis- permanent dilation of the bronchioles
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22
Q

Causes/ RFs of chronic bronchitis

A
  • 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)
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23
Q

CLinicl presentaitona nd definition of chronci bronchitis

A
  • 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
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24
Q

EMphysema - what is this

A
  • 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
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25
Q

Anatomcial classificaiton emphysema

A

Anatomical classification

In early stages good clue of the aetiology e.g smoking in centrilobular

But in advanced cases - mixed

26
Q

EMphysema in cystic fibrosis - how come

A

•Lack of alpha 1 anti trypsin allows unchecked action of proteolytic enzyme trypsin to damage tissue proteins in alveolar wall

27
Q

Complicaitons in Emphysema

A
  • Bullous emphysema > 1cm diameter
  • Interstitial emphysema- intra pulmonary leakage of air into the interstitium
  • Traumatic or spontaneous pneumothorax due to rupture of sub pleural bulla
28
Q

clinical presentaiton emphysema

A
  • Productive cough
  • Breathlessness

Infective Exacerbation

29
Q

Temrinal complicaiton of emphysema

A

Respiratory failure

30
Q

Extra Pulmonary complciatiosn of COAD and ILD

A
  • Secondary pulmonary hypertension- due to vascular remodelling as a result of hypoxia, inflammation and adaptive loss of capillaries in severe emphysema (adaptive to maladaptive response)
  • Proportional or in some patients out of proportion (disproportional)
  • Chronic cor pulmonale (CCP)- right heart disease secondary to lung disease- right ventricular hypertrophy following secondary pulmonary hypertension
  • Cardiac cirrhosis- liver fibrosis due to chronic passive venous congestion as a result of right heart dysfunction from CCP- reversed liver lobulation (from anatomical point )
31
Q

Bronchiolitis vs emphysema

A
32
Q
A
33
Q

What is minute ventilation

A
  • Tidal volume x Respiratory rate- ml/min
  • Increased in emphysema as alveolar elasticity recoil defect
  • Not increased in chronic bronchitis as there is obstructive pathology
34
Q

SPirometry - pulmonary/lung function test (PFT/LFT)

A
  • FVC- Forced vital capacity- Total volume exhaled in a forced exhalation following maximal inspiratory effort
  • FEV1- Fractional exhaled volume in the first second
35
Q

Obstructive vs restrictive pattern of lung disease on PEF

A
36
Q

Spirometry - graph - which side is osbtructive, which is restrictive

A
37
Q

COPD and compliance in the lungs

A
  • Lung compliance increases due to destruction of elastic in alveolar wall
  • But these cannot exhale/expire well
  • So gradual derecruitment over time reduces dynamic compliance
38
Q

What is compliance?

A

How easily the alveoli open with less work of respirstion

39
Q

Is expiration passive?

A

YES

40
Q

What is dynamic compliance

A

When air flows and it changes with time and flow

41
Q

Static complicance - what is this in lungs

A

Without air flow (less practical)

42
Q

Specific compliance in lungs- what si this

A

• actually relative compliance- comparison but there is no reference range as too many variables even in set population

43
Q

Presentation of Interstitial Lung diseases

A
  • Acute- in a variety of conditions leading to respiratory failure, often part of MODS (multiple organ dysfunction syndrome) or SIRS (systemic inflammatory response syndrome)
  • Shock, infection, DIC (disseminated intravascular coagulopathy), narcotics, poisonous gas inhalation etc
  • Chronic- breathlessness, restrictive pattern
  • May be defined clinical setting of exposure due to occupation or preoccupation/hobby
44
Q

What is the terminary pulmonary complication in interstitial lung diseases

A
  • End stage lung disease/honeycomb lung
  • Respiratory failure type II
  • Diffuse pulmonary fibrosis hinders gas exchange beyond limits of compensation
  • Ventilatory support
  • Lung transplant if modifiable factors or IPF
45
Q

Chronic clinical settings - interstitial lung diseases (occupational lung diseases)

A
  • Occupation- pneumoconiosis- coal workers, asbestos exposure (asbestosis), farmer’s lung (EAA)
  • Preoccupation/hobby- Extrinsic allergic alveolitis/EAA/hypersensitivity pneumonitis- e.g. Bird Fancier’s disease
  • Specific pathological entities- Sarcoidosis, Langerhans cell histiocytosis (LCH- cystic smoker’s lesion with specifIc biopsy features), alveolar proteinosis (characteristic HRCT and cytology), smokers (RB-ILD, respiratory bronchiolitis-interstitial lung disease- transition from COAD to ILD)
  • Acute presentation in known chronic setting
46
Q

Sarcoidosis (type intersitital lung disease)

A
  • Bihilar lymphadenopathy
  • Multisystem involvement
  • Reticulonodular shadow in HRCT (high resolution CT)
  • Raised ACE (angiotensin convertase enzyme)
  • Sudden death possible in cardiac involvement
  • Typically non necrotic granuloma with Schauman and asteroid bodies (lamellated and star shaped calcification due to chronicity)
47
Q

Sarcoidosis - pathology/cause (type interstitial lung disease)

A
48
Q

Langerhans cells hisyiocytosis (type of interstitial lung disease)

A
49
Q

ELectorn microscopy of Langerhans cell histiocytosis

A
50
Q

Alveolar Proteinosis (type interstitial lung disease)

A
51
Q

Coalw orkers penumoconiosis (type interstitial lung dissease)

A
52
Q

Asbestosis - Interstitial lung disease

A
53
Q

Idiopathic lung disease

A
  • Vast majority
  • Some may overlap
  • Idiopathic pulmonary fibrosis in asbestosis
  • ILD in COAD (RB-ILD)
  • Desquamative interstitial pneumonia (DIP) no longer considered a specific smoker’s ILD
54
Q

Unusual interstitial pnemonia

A
  • Clinically idiopathic pulmonary fibrosis
  • Characterised by subpleural involvement (spatial heterogeneity) and
  • Temporal heterogeneity (various stages of fibrosis- young cellular fibrous buds and established paucicellular old pink/hyaline fibrosis)
  • Intra alveolar young cellular fibrous buds- BOOP- bronchiolitis obliterans organizing pneumonia (smokers)
55
Q

Acute injury- ARDS (adult respiratory distress syndrome)

A
  • Similar to the hyaline membrane disease of the newborn due to surfactant deficiency or NRDS of any cause (neonatal respiratory distress syndrome)
  • Alveolar lining replaced by pink hyaline membrane
  • Hinders gas exchange beyond limits of compensation
  • If superadded fibrous foci or BOOP- AFOP (acute fibrinous and organizing pneumonia, William Travis)- seen in survivors or compensated groups
56
Q
A
57
Q

Cryptogenic organising penumonia

A
58
Q

Acuet fibrinous and organising pneumonia

A
59
Q

Unusual interstitial pneumonia of slide

A
60
Q

Overlap in repsirtory patho

A
  • COPD-Bronchial asthma overlap
  • UIP in asbestos exposed (not NSIP pattern, legally contested for compensation)
  • Endogenous pneumoconiosis- confusing term to denote iron encrustation of vessels in passive venous congestion and chronic cor pulmonale type pathology
61
Q

Lung transplant criteria, indicatiosn and contraindications

A
62
Q

Interstilial lung diseases

A

U17 + 18 (22 decks)

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