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Unit 18 Week 4 > Workshop: Respiratory System > Flashcards

Workshop: Respiratory System Flashcards

1
Q

What is dead space?

A
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2
Q

What is right to left shunt?

A
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3
Q

What is the diffusion defect?

A
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4
Q

What is ventilation perfusion V/Q mismatch?

A
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5
Q

What are the anatomical components of respiratory system?

A
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6
Q

Draw out the airways-respiratory tree

A
  • Lack of cartilage from terminal bronchiole- more distensible but vulnerable to compression
  • Hierarchical branching
  • Alveoli- exchanger unit
  • Before alveoli- conduits/thoroughfare
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7
Q

When is airway resistance highest and when does it fall?

A
  • Airway resistance is maximum at 5th-8th gen bronchi
  • It falls beyond the 10th gen
  • As increased cross section over-compensates for the progressive narrowing
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8
Q

What is present in lung parenchyma?

A
  1. Alveoli
  2. Alveolar interstitium
  3. Capillaries
  4. Alevolocapillary membranes
  5. Alveolocapillary interstitium
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9
Q

How much lung surface is there in the lungs and how many miles of airway is there?

A
  • Both lung surface is equal to a folded tennis court
  • With 1500 miles of airway running through it
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10
Q

What is the law of gas exchange?

A
  • Can only occur in the alveolus
  • That is both ventilated and perfused
  • Alveolocapillary membrane is key
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11
Q

Explain insufficiencies 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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12
Q

Explain physiological inefficiencies 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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13
Q

What are the functions of the lungs?

A
  1. Narrower than the functions of the respiratory system, as a whole, which also offers
  2. Speech and olfaction, humidification and temperature control, respiratory defence- gag, sneeze and cough
  3. Lungs- oxygenation, removal of waste gases e.g., CO2
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14
Q

What makes up respiratory failure?

A
  • Impaired ventilation- neuromuscular defect
  • Impaired perfusion- vascular defect
  • Impaired diffusion- intrinsic lung alveolar defect
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15
Q

Causes of impaired ventilation?

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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16
Q

What are some causes of impaired perfusion?

A
  • Cardiovascular- heart failure, multiple pulmonary emboli
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17
Q

What is the cause of impaired diffusion?

A

Diffuse parenchymal fibrosis

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18
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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19
Q

What is respiratory failure?

A
  • RF is defined as a condition in which there is failure in one or both of the gas exchange 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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20
Q

What are some physical signs of respiratory failure?

A
  • Dyspnoea
  • Somnolence
  • Headache
  • Confusion
  • Coma
  • Asterixis (flapping tremor/hepatic flap)
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21
Q

Explain V/Q mismatch

A
  • A hyperventilating normal alveolar unit cannot compensate for the hypoxaemia due 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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22
Q

What are some adaptations in V/Q 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)

A = alveolar

a - arterial

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23
Q

What is COPD describe?

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
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24
Q

Explain the pathology of chronic bronchitis (in COPD)

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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25
Q

What are the complications of chronic bronchitis?

A
  • Acute exacerbation
  • Bronchopneuminia
  • Bronchiectasis- permanent dilation of the bronchioles
26
Q

What are the causes/risk factors of COPD?

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)
27
Q

What s the clinical presentation of someone with COPD?

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
28
Q

What is emphysema?

A
  • Abnormal enlargement or dilation of the alveolar air space distal to the terminal bronchiole (get dilated air spaces)
  • 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
  • Anatomical classification
  • In early stages good clue of the aetiology e.g smoking in centrilobular
  • But in advanced cases - mixed

TB- terminal bronchiole, RB- respiratory bronchiole A- alveolus

29
Q

What does emphysema look like on histology?

A

Dilated air spaces

30
Q

Explain cystic fibrosis and emphysema

A
  • Lack of alpha 1 anti trypsin allows unchecked action of proteolytic enzyme trypsin to damage tissue proteins in alveolar wall
31
Q

What are some complications of 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

Terminal complication: respiratory failure

32
Q

What are clinical features of emphysema?

A
  • Productive cough
  • Breathlessness
  • Infective Exacerbation
33
Q

What are some extra-pulmonary complications of COPD 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 )
34
Q

What are the types of COPD patients and explain their clinical signs and symptoms?

A
35
Q

What are the types of COPD patients and explain their clinical signs and symptoms?

& complications

A
36
Q

Explain FVC

A

FVC- Forced vital capacity- Total volume exhaled in a forced exhalation following maximal inspiratory effort

37
Q

Explain FEV1

A
  • FEV1- Fractional exhaled volume in the first second
38
Q

Explain obstructive vs restrictive pattern for FVC, FEV1 and FEV1:FVC ratio

A
39
Q

Draw out spirometry graphs of obstructive and restrictive patterns

A
40
Q

Explain COPD and compliance

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
41
Q

What is compliance?

A
  • Compliance- how easily the alveoli open with less work of respiration
42
Q

What process is expiration?

A

Passive process

43
Q

What is dynamic compliance?

A

•Dynamic compliance- when air flows and it changes with time and flow

44
Q

What is static compliance?

A

•Static compliance- without air flow (less practical)

45
Q

What is specific compliance?

A

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

46
Q

How do interstitial lung diseases present acutely and chronically?

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
47
Q

What are some terminal pulmonary complications of ILD?

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
48
Q

Causes of ILD?

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
49
Q

What is sarcoidosis? & how does it present? and histology?

A

Sarcoidosis is a rare condition that causes small patches of red and swollen tissue, called granulomas, to develop in the organs of the body. It usually affects the lungs and skin

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)

50
Q

Explain Langerhans cell histiocytosis & clinical presentation and histology

A

What is it?

Langerhans cell histiocytosis is a disorder in which excess immune system cells called Langerhans cells build up in the body. Langerhans cells, which help regulate the immune system, are normally found throughout the body, especially in the skin , lymph nodes, spleen , lungs, liver , and bone marrow.

Clinical presentation

Typically smoker

Cystic lesion

Plenty of eosinophils

Grooved coffee bean nuclei

Cd1a, Langerin, S100, BRAF positive

(Immunohistochemistry)

Accessory cell lesions by the Histiocytic

Society

Classic electron microscopic findings

What is seen on histology?

  • Birbek granules/bodies
  • Tennis racket shaped inclusions
  • Not required in typical IHC
51
Q

Explain infection spread, genetic predispositioning, socio-economic predispositioning and environmental predispositioning of sarcoidosis

A
52
Q

Explain alveolar proteinosis and histology

A

What is it?

Pulmonary alveolar proteinosis (PAP) is a syndrome, a set of symptoms and signs – not a single disease, in which surfactant in alveoli builds up slowly. This blocks air from entering alveoli and oxygen from passing through into the blood, which results in a feeling of breathlessness (dyspnea).

Clinical presentation

Thyroidised lung

Alveoli drowned in proteinaceous material

Uncertain aetiology

Unknown pathogenesis

Some associated with haematological conditions

53
Q

Explain coal workers pneumoconiosis

A

Transilluminated lung slice

Black fibrotic nodules > 1 cm = progressive massive fibrosis (PMF)

Cavitation

COMPLICATED COAL WORKERS PNEUMOCONIOSIS

54
Q

Explain asbestosis and what it looks like

A

What is it?

Asbestosis is a serious lung condition caused by long-term exposure to asbestos. Asbestos is a fibre-like material that was once used in buildings for insulation, flooring and roofing. Its use has been fully banned in the UK since 1999. While asbestos can be dangerous, it’s not harmful if left alone.

Findings

Note irregular honeycombing

No particular site predilection

NSIP pattern- non specific interstitial pneumonia

Asbestos/ferruginous bodies and count

55
Q

Explain idiopathic pulmonary fibrosis

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
  • 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)
56
Q

What is 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
57
Q

Explain COP (cryptogenic organising pneumonia)

A

What is it?

Cryptogenic organizing pneumonia (COP) is a form of interstitial lung disease where the small airways (bronchioles) and alveoli (tiny air sacs) become inflamed, leading to difficulty breathing and flu-like illness.

Clinical findings

BOOP- bronchiolitis obliterans organizing pneumonia

Masson’s body

58
Q

Explain AFOP (acute fibrinous and organising pneumonia)

A

What is it?

Acute fibrinous and organizing pneumonia (AFOP) is a very rare form of acute or subacute lung injury, which is characterized by patches of “fibrin balls” distributed within the alveoli.

Clinical findings

Mixture of cellular organization/BOOP

And hyaline membranes/fibrin

59
Q

Match them up:

Clinical scenario:

  • Idiopathic pulmonary fibrosis
  • Acute opiate overdose
  • Patent foramen ovale
  • Cerebrovascular accident
  • COPD/COLD/COAD (chronic obstructive airway disease)

Type of defect and respiratory failure:

  • Diffusion defect, type II
  • Ventilation defect, type II
  • Perfusion defect, type I
  • Ventilation defect, type II
  • Complex mechanism, type II, see later
A

???????

60
Q

Match them up:

Clinical:

  • Idiopathic pulmonary fibrosis/IPF
  • Pneumoconiosis/asbestosis
  • Cryptogenic organizing fibrosis (COF)
  • Adult respiratory distress syndrome/ARDS

Pathological pattern:

  • Usual interstitial pneumonia (UIP)
  • Non-specific interstitial pneumonia(NSIP)
  • BOOP (bronchiolitis obliterans organizing pneumonia)
  • Diffuse alveolar damage(DAD)
A

??????

Unit 18 Week 4 (3 decks)

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