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Medical Studies 1 > Week 7 Respiratory > Flashcards

Week 7 Respiratory Flashcards

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USMLE® Step 1 flashcards
1
Q

restrictive vs obstructive lung disease

A

-restrictive lung disease is characterised by a reduction in lung volume whereas obstructive lung disease is caused by an airway obstruction (no change in lung volume)

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2
Q

what are the broad causes of restrictive lung disease

A

-pleural pathologies
-alveolar pathologies
-interstitial pathologies
-neuromuscular pathologies
-thoracic cage abnormality pathologies
(PAINT)

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3
Q

causes of interstitial vs extra pulmonary restrictive lung disease

A

-interstitial arises from conditions affecting the lung parenchyma such as fibrosis
-extrapulmonary arises from factors outside the lung that limit lung expansion such as obesity

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4
Q

examples of intrinsic restrictive lung diseases

A

-interstitial lung disease
-alveolar conditions (oedema)
-diffuse cellular infiltrates
-sarcoidosis, asbestosis

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5
Q

examples of extrinsic restrictive lung disease

A

-low respiratory muscle tone (neuromuscular)
-chest wall deformities (scoliosis, obesity)
-space occupying (pleural effusion)

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6
Q

list the symptoms of RLD

A

dyspnoea
cough
malaise
muscle weakness

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7
Q

why does RLD present with dyspnoea

A

reduced lung compliance and increased work of breathing, leading to SOB

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8
Q

why does RLD present with cough

A

increased interstitial lung tissue stiffness triggers cough reflex

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9
Q

why does RLD present with malaise

A

chronic hypoxia and reduced lung function causes systemic fatigue and general discomfort

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10
Q

why does RLD present with muscle weakness

A

prolonged hypoxia and respiratory muscle overuse leads to decreased muscle strength

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11
Q

list the physical exam findings of restrictive lung disease

A

-reduced chest expansion
-tachypnoea
-decreased breath sounds
-inspiratory crackles
-cyanosis

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12
Q

why does RLD present with reduced chest expansion

A

stiffened lung parenchyma restricts thoracic movement

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13
Q

why does RLD present with tachypnoea

A

increased respiratory rate compensates for reduced lung volume

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14
Q

why does RLD present with decreased breath sounds

A

reduced lung volume reduced airflow, leading to quieter breath sounds

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15
Q

why does RLD present with inspiratory crackles

A

alveolar and interstitial fibrosis causes popping sounds during inspiration due to the sudden opening of collapsed airways

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16
Q

why does RLD present with cyanosis

A

bluish discolouration of the skin and mucous membranes due to inadequate oxygenation

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17
Q

effect of RLD on ventilation

A

impaired ventilation due to the stiffening and reduced compliance of lung tissue which restricts lung expansion

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18
Q

effect of RLD on perfusion

A

thickening of the alveolar capillary membrane, common in RLD, hinders efficient gas exchange, prolonging time required for oxygen to diffuse into pulmonary capillaries

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19
Q

describe v/q mismatch as a hallmark feature of RLD

A

-mismatch in ventilation and perfusion can lead to areas of the lung receiving less oxygen than they should
-this can cause hypoxic vasoconstriction (directing blood away from poorly ventilated areas)
-chronically this can result in pulmonary hypertension and right heart strain

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20
Q

what is interstitial lung disease (ILD)

A

-disease which affects the lung interstitium (tissue of alveolar wall between the capillary endothelium and alveolar epithelium)
-ILD progress into irreversible pulmonary fibrosis

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21
Q

what is inorganic exposure ILD

A

lung disease caused by exposure to non-organic substances such as asbestos or silica

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21
Q

list the classifications of ILD

A

-inorganic exposure
-organic exposure
-smoking
-rare forms of ILD
-idiopathic

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22
Q

what is organic exposure to ILD

A

lung disease resulting form exposure to organic materials, like mould or bird droppings, which can trigger inflammation and scarring in lungs

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23
Q

what is smoking ILD

A

lung disease associated with the inhalation of toxins from tobacco smoke

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24
Q

what is rare form of ILD

A

uncommon types of ILD that may have unique causes or characteristics, requiring specialised diagnosis and treatment

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25
Q

what is idiopathic ILD

A

a term used to describe ILD with an unknown cause, indicates the conditions arises without an underlying trigger or cause

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26
Q

define occupational lung disease

A

diseases that affect the lung parenchyma because of occupational exposure to dust, fumes,smoke or biological agents

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27
Q

what are the types of occupational lung disease

A

asbestosis
mesothelioma
pleural disease

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28
Q

describe asbestosis

A

chronic lung disease caused by inhalation of asbestos fibres, resulting in lung scarring and impaired respiratory function

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29
Q

describe mesothelioma

A

rare and aggressive cancer that primarily affects the lining of lungs, abdomen or heart and is strongly associated with asbestos exposure

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30
Q

describe pleural disease

A

conditions affecting the pleura due to workplace exposures, can lead to pleuritis, pleural effusion and plaques

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31
Q

outline the pathophysiology of asbestos related RLD

A

-prolonged exposure to asbestos/inhalation of asbestos fibres
-DNA damage (mesothelioma)
-acute and chronic inflammation
-inflammation of lung parenchyma (pleural effusion)
-fibroblast activation
-collagen deposition
-pulmonary fibrosis
-decreased compliance of lung
-RLD
-lowered gas exchange
-dyspnoea

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32
Q

list the investigations for RLD

A

chest x ray
spirometry
ABG’s

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33
Q

what is found on chest x ray with RLD

A

-reduced lung volume with a flattened diaphragm
-increases opacity in lung fields due to decreased air
-could find: reticular opacities or ground-glass infiltrates

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34
Q

what is found on spirometry for RLD

A

-reduced lung volume
-decreases TLC,VC,FVC,
-normal/increased FEV1/FVC ratio (indicating restriction)

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35
Q

what is found on ABG for RLD

A

-reduced PaO2
-normal or low PaCO2 (can be high only if very severe)
-indicates little CO2 retention (pt is able to hyperventilate) but impaired O2 exchange

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36
Q

what are the way to manage RLD

A

-minimise exposures
-steroids (anti inflammatory)
-Lung transplant (high risk/reward)
-Pulmonary rehab (conditioning)
-Education

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37
Q

FEV/FEV1 in asthma

A

lowered

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38
Q

FEV/FEV1 in emphysema

A

lowered

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39
Q

TLC in ILD

A

lowered

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40
Q

DLCO in asthma

A

normal

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41
Q

DLCO in emphysema

A

lowered

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42
Q

DLCO in ILD

A

lowered

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43
Q

what are the defences of the respiratory system against infection

A

mucous layer
epithelium
lamina propria
type 1 penumoyctes
type 2 pneumocytes

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44
Q

how does the mucous layer provide protection for respiratory system

A

traps pathogens and/ore foreign particles; expels them via mucocilliary escalator

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45
Q

how does the epithelium provide protection for respirator system

A

contains goblet cells that secrete mucous; creates a physical barrier

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46
Q

how does lamina propria provide protection for the respiratory system

A

contains immune cells (macrophages,Dc)

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47
Q

how do type 1 pneumocytes provide protection for the respiratory system

A

physical barrier between the lung and the airway

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48
Q

how do type 2 pneumocytes provide protection for the respiratory system

A

secrete surfactant to protect the lung against collapse and/or infection

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49
Q

what substances can be released to compromise respiratory defence

A

microbes
DAMPs
Foreign bodies

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50
Q

how do DAMPS compromise respiratory defence

A

released from damaged cells, enters lungs and causes stress

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51
Q

how do foreign bodies compromise respiratory defence

A

triggers hypersensitivity reactions and/or causes chemical injury

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52
Q

what are the causes of compromised immunity

A

defective mucosa
dysfunctional cillia
immune cell defects

53
Q

how does defective mucous compromise immunity

A

inability for the lung to trap/remove pathogens (eg cystic fibrosis)

54
Q

how does dysfunctional cilia compromise immunity

A

dysfunction caused by smoking or drug use

55
Q

how do immune cells defects compromise immunity

A

impaired action of cells means less immune action

56
Q

what are the common causes of lung inflammation

A

infection
pollutants
allergens
foreign bodies
autoimmune
occupational
lifestyle

57
Q

List the process of acute pulmonary inflammation

A
  1. recognition of threats
  2. activation of innate immunity
  3. activation of adaptive immunity
    4.repair phase
58
Q

describe step 1 (recognition of threats) in acute pulmonary inflammation

A

-immune cells detect pathogens and damage through pattern recognition receptors (PRRs), such as Toll-like (TLRs) and NOD-like receptors (NLR’s)
- These receptors identify microbial and non-pathogenic threats, initiating the immune response.

59
Q

describe step 2 (activation of innate immunity) in acute pulmonary inflammation

A

-macrophages, dendritic cells, and innate lymphoid cells recognise pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs)
-releasing cytokines (e.g., IL-6, TNF) to promote inflammation and recruit additional immune cells to the site.

60
Q

describe step 3 (activation of adaptive immunity) in acute pulmonary inflammation

A

-Dendritic cells and B cells present pathogen fragments to T cells,
-activating CD8+ T cells to kill infected cells and CD4+ T cells to help B cells produce antibodies (IgG) for pathogen neutralization and long-term immunity.

61
Q

describe step 4 (repair phase) in acute pulmonary inflammation

A

Damaged tissue is cleaned by macrophages and fluid is resorbed by lymphatics,
while TGF-beta-induced fibrosis and type II pneumocyte proliferation restore the alveolar lining and repair tissue integrity.

62
Q

Outline the process of chronic pulmonary inflammation

A

-immune cells persistently detect and respond to prolonged/repetitive stimuli through pattern recognition receptors (continuous
activation)
-resolution process aims to resolve inflammation through mechanisms that counter inflammation
-remodeling occurs due to persistent inflammation, chronic damage results in structural changes and fibrosis as tissue attempts to repair and adapt

63
Q

Give a brief overview of TB

A

-Mycobacterium tuberculosis bacteria are inhaled and enter
the lungs, where they are engulfed by alveolar macrophages
-bacteria resist destruction, replicate, and form granulomas (tubercles) to contain the infection.
-Progression of the disease leads to caseous necrosis in the granuloma, characterised by cheese-like tissue destruction
-The immune response can cause lung damage and fibrosis, impairing respiratory function.

(in some cases, the
bacteria can spread from the lungs to other organs via the bloodstream, causing extrapulmonary TB.)

64
Q

describe the anatomy of a granuloma

A

-A granuloma is an organised cluster of macrophages that transform into epithelioid cells.
-These cells are surrounded by lymphocytes and occasionally multinucleated giant cells (from macrophage fusion).
-The centre may show caseous necrosis (cheese-like tissue due to cell death).
-Fibroblasts and collagen can form a fibrous capsule around the granuloma.
-Granulomas are common in chronic inflammation (e.g., TB) and help isolate persistent pathogens or irritants.

65
Q

what is the test for TB

A

Mantoux test

66
Q

features of Mantoux test

A

-detect the delayed-type hypersensitivity (IV) by injecting a small amount of a targeted antigen intradermally
-then observing
the reaction, which indicates prior exposure and sensitisation to the pathogen.

67
Q

link alveoli inflammation to relevant symptoms

A

inflammation impairs gas exchange –> SOB, hypoxemia

68
Q

link interstitium inflammation to relevant symptoms

A

inflammation reduce lung compliance and gas exchange –> chronic dry cough and progressive dyspnoea

68
Q

link bronchi inflammation to relevant symptoms

A

inflammation leads to swelling and mucous production –> cough, wheezing and difficulty breathing

69
Q

link parenchyma inflammation to relevant symptoms

A

inflammation affects overall lung function -> decreased LV , fatigue and exercise intolerance

70
Q

other names for the common cold

A

non specific URTI, acute coryza, acute infective rhinitis

71
Q

what causes colds

A

viruses (unless secondary bacterial infection-2%)

72
Q

list the management for colds

A

antivirals and antibiotics

73
Q

most common antiviral

A

oseltamivir

74
Q

what is pharyngitis

A

condition characterised by inflammation of the pharynx

75
Q

symptoms of pharyngitis

A

-coryzal (cold) symptoms: runny nose, cough
-can present with conjunctivitis

76
Q

broad causes of pharyngitis

A

-viruses mostly (Epstein Barr virus)
-1/3 cases are bacterial (Strep A)
-GORD, allergies, chemotherapy (rare)

77
Q

list the complications of pharyngitis

A

-peritonsillar abscess
-deep neck space infection
-rheumatic fever
-glomerulonephritis
-scarlet fever

78
Q

what is peritonsilar abscess

A

a collection of pus near the tonsils causing severe throat pain and difficulty swallowing

79
Q

what is deep neck space infection

A

a serious infection spreading to deep tissues in the neck, potentially affecting breathing and swallowing

80
Q

what is rheumatic fever

A

an inflammatory condition that follows strep pharyngitis, affecting heart, joints, brain and skin

81
Q

what is glomerulonephritis

A

kidney inflammation that can develop after strep infection, leading to haematuria and HTN

82
Q

what is scarlet fever

A

condition characterised by red, sandpaper like rash and high fever, typically only follows from strep pharyngitis

83
Q

List the management for pharyngitis

A

-assess for life threatening features
-antibiotics
-tonsillectomy

84
Q

describe assessing for life threatening features in pharyngitis

A

check for airway obstruction, deep neck space infection, sepsis

85
Q

describe antibiotics use for pharyngitis

A

if suspected bacterial cause, administered in high risk rheumatic fever cases, also used for severe symptoms, not improving after 3-7 days, or immunosuppressed

86
Q

describe tonsillectomy use for pharyngitis

A

consider for recurrent significant pharyngitis, refer if >7 episodes per year, >5 episodes/year for 2 years or >3 episodes/year for 3 years

87
Q

features of laryngitis

A

-inflammation of larynx
-almost always viruses
-usually self limiting, treat with analgesia, steam inhalation
-no improvement after a month=seek ENT

88
Q

what is epiglottitis

A

cellulitis of the epiglottis and surrounding tissues, leading to life threatening airway obstruction

89
Q

symptoms and signs of epiglottitis

A

-sudden onset: high fever, respiratory distress and stridor
-appears toxic, anxious or drooling
-neck hyperextension and tripod position

90
Q

list the management for epiglottitis

A

-secure airway
-limit intervention
-antibiotic therapy

91
Q

what does securing the airway entail for epiglottis

A

prioritising airway management (specialist must be involved)

92
Q

what does limiting intervention mean for epiglottitis

A

avoid procedures that could worsen the condition before expert help is available

93
Q

what does antibiotic therapy entail for epiglottitis

A

give IV antibiotics (3rd gen cephalosporin) with steroids if needed

94
Q

what is acute otitis media (AOM)

A

-condition characterised by presence of fluid in the middle ear, along with dysfunction of the eustachian tube

95
Q

what causes acute otitis media (AOM)

A

viruses and bacteria (strep pneumoniae) cause it

96
Q

symptoms of acute otitis media

A

ear pain, hearing loss, fever, lethargy and ear discharge (if ear drum bursts)

97
Q

how do you diagnose AOM

A

otoscopy and sometimes microbiological testing

98
Q

list the complications of AOM

A

-OME (otitis media with effusion)
-CSOM (chronic supparative otitis media)
-mastoditis

99
Q

describe OME as a complication of AOM

A

persistent fluid in the middle ear following an infection, often resolving within 3 months, with tympanostomy tubes required for prolonged cases with hearing loss

100
Q

describe CSOM as a complication of AOM

A

long term ear infection caused by a perforated tympanic membrane and purulent drainage lasting over 6 weeks, managed with aural toilet and topical drops, with surgery reserved for recurrent or refractory causes

101
Q

describe mastoidits as a complication of AOM

A

spread of infection into mastoid air cells of temporal bone, causes erythema, swelling and pin

102
Q

Outline AOM management

A

-symptomatic treatment (analgesic)
-antibiotics (amoxicillin) are required if pt is under 6 months of age, has bilateral infections, perforated tympanic membrane, ATSI, immunocompromised
-antibiotics shorten symptoms (more than 24 hrs needed)

103
Q

what is acute sinusitis

A

inflammation of the paranasal sinuses

104
Q

symptoms and signs of acute sinusitis

A

-severe nasal congestion
-prurulent nasal discharge
-facial pain
-maxillary tooth pain
-loss of smell

105
Q

causes of acute sinusitis

A

-most cases are viral
-bacterial infections (which are rare) can involve (Strep.pneumoniae, S.aurues)

106
Q

contrast acute and chronic sinusitis

A

Acute sinusitis is defined by symptoms lasting less than four weeks, while chronic sinusitis persists for more
than twelve weeks, often linked to allergies.

107
Q

Outline the management of acute sinusitis

A

-treatments include analgesics and decongestants to relieve pain and congestion
-nasal saline irrigation to clear mucous
-antibiotics for bacterial cases
-avoid blowing nose hard
-more surgery and targeted treatments could be required for fungal infections in immunosuppressed patients

108
Q

what are NSCLC and SCLC

A

non small cell lung cancer and small cell lung cancer

109
Q

contrast prevalence of NSCLC and SCLC

A

NSCLC: Most common, 85% of lung cancers.
SCLC: Less common, 10-15%, but more aggressive.

110
Q

contrast the cellular origin of NSCLC and SCLC

A

NSCLC: From epithelial cells, with subtypes including adenocarcinoma, squamous cell carcinoma, and large cell carcinoma.
SCLC: From neuroendocrine cells, with rapid growth and metastasis.

111
Q

contrast growth and spread of NSCLC and SCLC

A

NSCLC: Slower growth, stays localized longer.
SCLC: Rapid spread, often to brain, liver, and bones.

112
Q

contrast prognosis of NSCLC and SCLC

A

NSCLC: Better survival, depends on stage.
SCLC: Poor prognosis, diagnosed late.

113
Q

contrast biomarkers of NSCLC and SCLC

A

NSCLC: Targetable genetic mutations (EGFR, ALK, KRAS).
SCLC: Fewer actionable mutations, mainly treated with chemotherapy.

114
Q

List Personal risk factors for lung cancer

A

-Current or past smoking – estimated to account for 90%
* 10-30 fold increase in relative risk to non-
smokers
* Age
* Family history of lung cancer
* COPD
* Pulmonary fibrosis
* Personal history of lung cancer

115
Q

List environmental and occupational risk factors for lung cancer

A

-Passive smoking
* Air pollution
* Occupational exposures –
asbestos, silica, diesel exhaust

116
Q

Signs and symptoms of lung cancer

A
  • New or changed cough
  • Chest/shoulder pain
  • Hoarse voice
  • Loss of weight or appetite
  • Recurrent/persistent chest infection
  • Lymphadenopathy
  • Haemoptysis
117
Q

signs of progressive disease (lung cancer)

A
  • Pleural effusion
  • Chest wall pain
  • Signs of metastasis (bone pain, neuro)
118
Q

List the investigations for lung cancer

A
  • CBE
  • Electrolytes
  • Calcium
  • Liver function tests
  • Albumin
  • Lactate dehydrogenase
  • Chest X-ray
  • CT chest
  • PET scan

*Biopsy

  • +/- CT head/abdomen/pelvis
119
Q

how is CT used for lung cancer Dx

A

Provides detailed cross-sectional images of the lungs, identifying the size, shape, and location of tumours, and evaluating lymph nodes and possible metastasis.

120
Q

how is PET used to Dx lung cancer

A

Used to detect metabolic activity of cancer cells, helping in staging and detecting metastasis.

121
Q

What biopsy is used to Dx lung cancer

A

-Bronchoscopy
-CT guided transthoracic biopsy (through the skin)
-Pleural aspirate

122
Q

What does TNM stand for

A

Tumour size and extent
Lymph node involvement
Metastasis

123
Q

Identify the management of NSCLC

A

Early stage – Surgery
Later stages – systemic treatment with chemo/radiotherapy

124
Q

Features of obstructive lung disease

A

-Alveoli: Hyperinflated (e.g., COPD).
-Lung Volumes: Increased total lung capacity (TLC) and residual volume (RV) due to air trapping.
-Breathing: Difficulty fully exhaling.
-Compliance: Increased due to loss of elastic recoil.
-FEV1/FVC Ratio: Decreased (less than 70%).
-FEV1: Markedly reduced.
-FVC: Reduced, but less than FEV1.
-TLC & RV: Increased.

“Imagine trying to blow air out of a balloon that has lost some of its elasticity”

125
Q

Features of restrictive lung disease

A

-Alveoli: Intact but limited in expansion.
-Lung Volumes: Decreased TLC, RV, and all other lung volumes.
-Breathing: Difficulty fully inhaling.
-Compliance: Decreased due to fibrosis or external restrictions.
-FEV1/FVC Ratio: Normal or increased (both
-FEV1 and FVC are reduced FEV1: Reduced, but in proportion to FVC.
-FVC: Markedly reduced.
-TLC & RV: Decreased.

Now, imagine a very stiff, small balloon that’s hard to inflate in the first place

126
Q

features of extrinsic RLD

A

-dyspnoea present
-no cough
-other systems effected
-normal gas exchange capacity
-type 2 resp failure
-normal HRCT chest

127
Q

features of intrinsic RLD

A

-dyspnoea present
-cough present
-other systems not effected
-decreased gas exchange capacity
-type 1 resp failure
-abnormal HRCT chest

128
Q

why does intrinsic RLD not lead to T2 respiratory failure

A
  • Intrinsic RLD affects lung tissue, impairing oxygen diffusion.
  • Leads to Type 1 respiratory failure (low oxygen)
  • CO₂ is still expelled due to easier diffusion.
  • Patients compensate by breathing faster, preventing CO₂ buildup.
  • Hypoxemia occurs without significant hypercapnia.
  • Unlike extrinsic RLD, which restricts ventilation and causes CO₂ retention, intrinsic RLD affects oxygenation more than CO₂ clearance.
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Medical Studies 1 (15 decks)

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