SEARCH RESULTS FOR: cystic fibrosis
Cystic Fibrosis
![](http://calgaryguide.ucalgary.ca/wp-content/uploads/2014/09/Cystic-Fibrosis.jpg)
Bronchiectasis Pathogenesis and clinical findings
![Bronchiectasis: Pathogenesis and clinical findings
Acquired immunodeficiency Lymphoma, HIV, transplant
Autoimmune Lupus, inflammatory bowel disease, rheumatoid arthritis
Congenital/Genetic Cystic fibrosis, A1AT deficiency, Marfan, immunoglobulin deficiency, Kartagener syndrome, Young syndrome
Endobronchial obstruction Neoplasm, foreign body, lymph node compression
Other Inhalation exposure (smoke, ammonia), MAC complex infection, COPD, allergic bronchopulmonary aspergillosis, chronic infections
Irreversibly dilated bronchi
Chronic bronchial infection and inflammation
1
Easily collapsible airways
I Bronchiectasis (persistent and progressive damage to lungs)
Chronic cough (mucopurulent)
Defect in immunity and/or mucus clearance
Persistent bacteria in airway (commonly Pseudomonas/Staph aureus)
Inflammatory response
Rhinosinusitis
Abbreviations: • A1AT — Alpha-1-antitrypsin • COPD — Chronic Obstructive Pulmonary Disease • HIV — Human Immunodeficiency Virus • MAC — Membrane Attack Complex • VQ— Ventilation/Perfusion ratio
Legend:
Pathophysiology Mechanism
Fever
Sign/Symptom/Lab Finding
Failure to thrive (children)
Authors: Rebecca (Becky) Phillips Reviewers: Midas (Kening) Kang Usama Malik Eric Leung* * MD at time of publication
Notes: • Can be focal (single lobe/segment) or diffuse (both lungs) • Mainly in elderly • 1% prevalence in children
Tissue damage
Epithelial destruction of airways
Further impairment of bacterial clearance
Persistent inspiratory adventitious sounds (crackles > wheezing)
Complications
Structural damage to bronchial walls
Obstructive pulmonary function tests
Hemoptysis
Chest pain
VQ mismatch and 4, gas exchange
4, oxygenation
Digital clubbing (rare)
Fatigue Dyspnea
Cyanosis (uncommon) Bronchiectasis: Pathogenesis and clinical findings
Acquired immunodeficiency Lymphoma, HIV, transplant
Autoimmune Lupus, inflammatory bowel disease, rheumatoid arthritis
Congenital/Genetic Cystic fibrosis, A1AT deficiency, Marfan, immunoglobulin deficiency, Kartagener syndrome, Young syndrome
Endobronchial obstruction Neoplasm, foreign body, lymph node compression
Other Inhalation exposure (smoke, ammonia), MAC complex infection, COPD, allergic bronchopulmonary aspergillosis, chronic infections
Irreversibly dilated bronchi
Chronic bronchial infection and inflammation
1
Easily collapsible airways
I Bronchiectasis (persistent and progressive damage to lungs)
Chronic cough (mucopurulent)
Defect in immunity and/or mucus clearance
Persistent bacteria in airway (commonly Pseudomonas/Staph aureus)
Inflammatory response
Rhinosinusitis
Abbreviations: • A1AT — Alpha-1-antitrypsin • COPD — Chronic Obstructive Pulmonary Disease • HIV — Human Immunodeficiency Virus • MAC — Membrane Attack Complex • VQ— Ventilation/Perfusion ratio
Legend:
Pathophysiology Mechanism
Fever
Sign/Symptom/Lab Finding
Failure to thrive (children)
Authors: Rebecca (Becky) Phillips Reviewers: Midas (Kening) Kang Usama Malik Eric Leung* * MD at time of publication
Notes: • Can be focal (single lobe/segment) or diffuse (both lungs) • Mainly in elderly • 1% prevalence in children
Tissue damage
Epithelial destruction of airways
Further impairment of bacterial clearance
Persistent inspiratory adventitious sounds (crackles > wheezing)
Complications
Structural damage to bronchial walls
Obstructive pulmonary function tests
Hemoptysis
Chest pain
VQ mismatch and 4, gas exchange
4, oxygenation
Digital clubbing (rare)
Fatigue Dyspnea
Cyanosis (uncommon)](http://calgaryguide.ucalgary.ca/wp-content/uploads/2018/02/Bronchiectasis-Pathogenesis-and-clinical-findings.png)
Sinusitis: Pathogenesis and clinical findings
![Sinusitis: Pathogenesis and clinical findings
Authors: Amanda Marchak Reviewers: Nicola Adderley Jim Rogers Danielle Nelson* * MD at time of publication
Abbreviations
URTI – Upper respiratory tract infection
Nasal obstruction/ congestion
Hyposmia
Headache
Facial pain/pressure
Maxillary tooth pain
Ear pain/ fullness
Osteomyelitis of frontal bone
Chemical irritants
Cystic Fibrosis
Direct toxic effect on cilia
Viral URTI Allergies
Inflammation of paranasal sinuses
Edematous passageways
Septal deviation Adenoid hypertrophy Polyps
Turbinate hypertrophy Tumors Foreign body
Dysfunctional cilia
Congenital and/or craniofacial abnormality Obstruct sinus ostia
Cilia unable to clear mucus from sinuses
Mucus unable to drain through ostia
Post-nasal drip Mucus overflows from the sinuses Cough
Mucus accumulates in sinuses
Occupies a larger volume
Applies ↑ pressure to sinus walls
Mucopurulent discharge
Bacterial1 overgrowth in sinuses Bacterial infection spreads to adjacent structures
Halitosis Pharyngitis Throat clearing
Dental root infection
Immunodeficiency
Note:
Irritates the back of the throat
Perforation of the Schneiderian membrane2
Passage of bacteria into the sinuses
Fever
Fatigue
Subperiosteal orbital abscess
Orbital abscess Orbital edema
↑ susceptibility to bacteria
1. The most common bacteria are Streptococcus pneumoniae, Haemophilus influenza, and Moraxella catarrhalis. Staphylococcus aureus and Group A Streptococcus may be seen, but are less common. However, in cases of dental root infection, oral anaerobes become more common, while Pseudomonas species are associated with foreign bodies.
2. The Schneiderian membrane is the membranous lining of the maxillary cavity.
Cavernous sinus thrombosis
Meningitis Cerebral abscess
Subdural abscess Epidural abscess
Periorbital or orbital cellulitis
Legend:
Pathophysiology
Mechanism
Sign/Symptom/Lab Finding
Complications
Published November 5, 2018 on www.thecalgaryguide.com
Sinusitis: Pathogenesis and clinical findings
Authors: Amanda Marchak Reviewers: Nicola Adderley Jim Rogers Danielle Nelson* * MD at time of publication
Abbreviations
URTI – Upper respiratory tract infection
Nasal obstruction/ congestion
Hyposmia
Headache
Facial pain/pressure
Maxillary tooth pain
Ear pain/ fullness
Osteomyelitis of frontal bone
Chemical irritants
Cystic Fibrosis
Direct toxic effect on cilia
Viral URTI Allergies
Inflammation of paranasal sinuses
Edematous passageways
Septal deviation Adenoid hypertrophy Polyps
Turbinate hypertrophy Tumors Foreign body
Dysfunctional cilia
Congenital and/or craniofacial abnormality Obstruct sinus ostia
Cilia unable to clear mucus from sinuses
Mucus unable to drain through ostia
Post-nasal drip Mucus overflows from the sinuses Cough
Mucus accumulates in sinuses
Occupies a larger volume
Applies ↑ pressure to sinus walls
Mucopurulent discharge
Bacterial1 overgrowth in sinuses Bacterial infection spreads to adjacent structures
Halitosis Pharyngitis Throat clearing
Dental root infection
Immunodeficiency
Note:
Irritates the back of the throat
Perforation of the Schneiderian membrane2
Passage of bacteria into the sinuses
Fever
Fatigue
Subperiosteal orbital abscess
Orbital abscess Orbital edema
↑ susceptibility to bacteria
1. The most common bacteria are Streptococcus pneumoniae, Haemophilus influenza, and Moraxella catarrhalis. Staphylococcus aureus and Group A Streptococcus may be seen, but are less common. However, in cases of dental root infection, oral anaerobes become more common, while Pseudomonas species are associated with foreign bodies.
2. The Schneiderian membrane is the membranous lining of the maxillary cavity.
Cavernous sinus thrombosis
Meningitis Cerebral abscess
Subdural abscess Epidural abscess
Periorbital or orbital cellulitis
Legend:
Pathophysiology
Mechanism
Sign/Symptom/Lab Finding
Complications
Published November 5, 2018 on www.thecalgaryguide.com](http://calgaryguide.ucalgary.ca/wp-content/uploads/2018/11/Sinusitis_Final.jpg)
cystic-fibrosis-findings-on-chest-x-ray-and-lung-window-ct-scan
![Cystic Fibrosis: Findings on Chest X-Ray and Lung Window CT Scan CFTR mutationàabnormal transmembrane Cl- transport in exocrine tissueà
Author: Sean Kennedy Reviewers: Matthew Harding, Amogh Agrawal, Yan Yu, Ciara
Hanly, Aman Wadhwani, Zesheng Ye (), Mark Montgomery* * MD at time of publication
Collapsed alveoli appears white on x-ray
Peribronchial Cuffing
secretions become more viscous. (See relevant slide for CF pathogenesis.)
As early as at birth, secretions collect in bronchial lumen, delaying mucociliary clearance
Mucus plugs and obstructs bronchial lumen
Air trapped distal to obstruction and cannot leave lungs
Lung Hyperinflation
Diaphragm domes below 10th posterior rib and 6th anterior rib on PA CXR
Flattened hemidiaphragm, enlarged retrosternal space on lateral CXR
With time, pulmonary capillaries gradually absorb gases in alveoli distal to obstruction àalveolar collapse (Atelectasis)
Collapsed alveoli more solid and radiodense than airà↓X-ray penetration
Adjacent structures may shift towards atelectasis on CXR
In first few years of life, retained bronchial secretions serve as nidus for recurrent bacterial colonization and infection
Late findings at 10- 30 years oldà secretion accumulation blocks inhaled air to affected lung segments àchronic hypoxia
Inflammatory response (cytokines, nitric oxide and radical oxygen species) leads to bronchial and peribronchial destruction
Hypoxia induces pulmonary capillary vasoconstriction
Some airways are blocked more than others
Leakage of fluid into bronchial walls & peri- bronchial regions.
Inflammatory cytokines destroy elastic components of bronchi
Accumulation of inflammatory exudate in bronchi
Pulmonary artery hypertension à Blood backs up in pulmonary arteries
Some segments of lung underventilated
Fluid around bronchial walls is more radiodense than air à↓X-ray penetration àappears white
Bronchiectasis: dilated, thickened, untapered bronchi on CXR/CT
Fluid/mucus in bronchi is more radiodense than air, thus appearing white on imaging
Edematous bronchi viewed end on are thickened and appear ring-like on CT/CXR
Tramlines (AKA Tramtracking)
Bronchus wider than corresponding blood vessel on CXR/CT
Advanced bronchiectasis is saccular in appearance
Mucus-filled bronchi form tubular opacities giving appearance of white fingers on CXR/CT
Signet Ring Sign
Bronchiectatic Cavities
Mucoid Impaction (AKA Finger in glove sign)
↑ Blood dilates pulmonary arteries
Blood backs up in right ventricle, dilating it
Pulmonary arteries look wider on CXR.
Main pulmonary artery >30 mm diameter on CT
Right Ventricle Enlargement on CXR/CT
Underventilated lung segments appear as lower intensity (darker) than normal ventilated segments which appear as normal intensity (brighter)
Mosaic Changes on CT(non- contrast
Legend:
Pathophysiology
Mechanism
Sign/Symptom/Lab Finding
Complications
Published June 13, 2013, updated Aug 18, 2021 on www.thecalgaryguide.com
Cystic Fibrosis: Findings on Chest X-Ray and Lung Window CT Scan CFTR mutationàabnormal transmembrane Cl- transport in exocrine tissueà
Author: Sean Kennedy Reviewers: Matthew Harding, Amogh Agrawal, Yan Yu, Ciara
Hanly, Aman Wadhwani, Zesheng Ye (), Mark Montgomery* * MD at time of publication
Collapsed alveoli appears white on x-ray
Peribronchial Cuffing
secretions become more viscous. (See relevant slide for CF pathogenesis.)
As early as at birth, secretions collect in bronchial lumen, delaying mucociliary clearance
Mucus plugs and obstructs bronchial lumen
Air trapped distal to obstruction and cannot leave lungs
Lung Hyperinflation
Diaphragm domes below 10th posterior rib and 6th anterior rib on PA CXR
Flattened hemidiaphragm, enlarged retrosternal space on lateral CXR
With time, pulmonary capillaries gradually absorb gases in alveoli distal to obstruction àalveolar collapse (Atelectasis)
Collapsed alveoli more solid and radiodense than airà↓X-ray penetration
Adjacent structures may shift towards atelectasis on CXR
In first few years of life, retained bronchial secretions serve as nidus for recurrent bacterial colonization and infection
Late findings at 10- 30 years oldà secretion accumulation blocks inhaled air to affected lung segments àchronic hypoxia
Inflammatory response (cytokines, nitric oxide and radical oxygen species) leads to bronchial and peribronchial destruction
Hypoxia induces pulmonary capillary vasoconstriction
Some airways are blocked more than others
Leakage of fluid into bronchial walls & peri- bronchial regions.
Inflammatory cytokines destroy elastic components of bronchi
Accumulation of inflammatory exudate in bronchi
Pulmonary artery hypertension à Blood backs up in pulmonary arteries
Some segments of lung underventilated
Fluid around bronchial walls is more radiodense than air à↓X-ray penetration àappears white
Bronchiectasis: dilated, thickened, untapered bronchi on CXR/CT
Fluid/mucus in bronchi is more radiodense than air, thus appearing white on imaging
Edematous bronchi viewed end on are thickened and appear ring-like on CT/CXR
Tramlines (AKA Tramtracking)
Bronchus wider than corresponding blood vessel on CXR/CT
Advanced bronchiectasis is saccular in appearance
Mucus-filled bronchi form tubular opacities giving appearance of white fingers on CXR/CT
Signet Ring Sign
Bronchiectatic Cavities
Mucoid Impaction (AKA Finger in glove sign)
↑ Blood dilates pulmonary arteries
Blood backs up in right ventricle, dilating it
Pulmonary arteries look wider on CXR.
Main pulmonary artery >30 mm diameter on CT
Right Ventricle Enlargement on CXR/CT
Underventilated lung segments appear as lower intensity (darker) than normal ventilated segments which appear as normal intensity (brighter)
Mosaic Changes on CT(non- contrast
Legend:
Pathophysiology
Mechanism
Sign/Symptom/Lab Finding
Complications
Published June 13, 2013, updated Aug 18, 2021 on www.thecalgaryguide.com](https://calgaryguide.ucalgary.ca/wp-content/uploads/2021/08/Cystic-Fibrosis-Findings-on-CT-CXR_2021.jpg)
copd-overview-and-definitions
![Defining “Chronic Obstructive Pulmonary Disease (COPD)”
Author: Yan Yu Reviewers: Jason Baserman, Jennifer Au, Ciara Hanly, Zesheng Ye (叶泽生), Yonglin Mai (麦泳琳)*, Naushad Hirani*, Juri Janovcik* * MD at time of publication
Cystic Fibrosis
Multisystem disease due to CFTR gene mutation, that presents in the lungs as bronchiectasis
Bronchiectasis, Cystic Fibrosis, etc
COPD
Systemic disease, largely manifesting as an airflow-obstructing respiratory disorder; can manifest in the form of any of the following disorders:
Emphysema
Lung tissue destruction & abnormal, permanent enlargement of lung acini: airspaces distal to terminal bronchioles
Chronic Bronchitis
Chronic, productive cough for a total duration of 3 months per year, over 2 continuous years
Asthma
Asthma that does not
remit completely with treatment (thus, chronic airflow obstruction) is defined as asthma-COPD overlap syndrome (ACOS)
Emphysema
Bronchiectasis
Destruction and widening of large airways, resulting in mucus hyper-secretion and recurrent infections
Chronic Bronchitis
Most common COPD manifestations
(most patients suffer from a combination of emphysema and chronic bronchitis)
Clinically, COPD is seen as:
• Progressive, partially reversible airflow obstruction and lung hyperinflation (causing respiratory symptoms like cough, sputum production, and dyspnea)
• Post-bronchodilator spirometry results: FEV1/FVC ratio <0.7 (FEV1 is not a defining feature of COPD, but a marker of severity)
• ↑ frequency & severity of acute exacerbations
• Systemic manifestations such as
deconditioning and muscle weakness
Chronic Obstructive Pulmonary Disease (COPD)
Asthma
Legend:
Pathophysiology
Mechanism
Sign/Symptom/Lab Finding
Complications
Published January 7, 2013, updated October 5, 2021 on www.thecalgaryguide.com
Defining “Chronic Obstructive Pulmonary Disease (COPD)”
Author: Yan Yu Reviewers: Jason Baserman, Jennifer Au, Ciara Hanly, Zesheng Ye (叶泽生), Yonglin Mai (麦泳琳)*, Naushad Hirani*, Juri Janovcik* * MD at time of publication
Cystic Fibrosis
Multisystem disease due to CFTR gene mutation, that presents in the lungs as bronchiectasis
Bronchiectasis, Cystic Fibrosis, etc
COPD
Systemic disease, largely manifesting as an airflow-obstructing respiratory disorder; can manifest in the form of any of the following disorders:
Emphysema
Lung tissue destruction & abnormal, permanent enlargement of lung acini: airspaces distal to terminal bronchioles
Chronic Bronchitis
Chronic, productive cough for a total duration of 3 months per year, over 2 continuous years
Asthma
Asthma that does not
remit completely with treatment (thus, chronic airflow obstruction) is defined as asthma-COPD overlap syndrome (ACOS)
Emphysema
Bronchiectasis
Destruction and widening of large airways, resulting in mucus hyper-secretion and recurrent infections
Chronic Bronchitis
Most common COPD manifestations
(most patients suffer from a combination of emphysema and chronic bronchitis)
Clinically, COPD is seen as:
• Progressive, partially reversible airflow obstruction and lung hyperinflation (causing respiratory symptoms like cough, sputum production, and dyspnea)
• Post-bronchodilator spirometry results: FEV1/FVC ratio <0.7 (FEV1 is not a defining feature of COPD, but a marker of severity)
• ↑ frequency & severity of acute exacerbations
• Systemic manifestations such as
deconditioning and muscle weakness
Chronic Obstructive Pulmonary Disease (COPD)
Asthma
Legend:
Pathophysiology
Mechanism
Sign/Symptom/Lab Finding
Complications
Published January 7, 2013, updated October 5, 2021 on www.thecalgaryguide.com](https://calgaryguide.ucalgary.ca/wp-content/uploads/2021/10/COPD-Overview-and-Definitions-2021.jpg)
Pediatric Pneumonia Pathogenesis and Clinical Findings
![Pediatric Pneumonia: Pathogenesis and clinical findings
Authors: Jasmine Nguyen Nicola Adderley Reviewers: Midas (Kening) Kang Usama Malik Annie Pham Eric Leung* Jean Mah* * MD at time of publication
Immunological: unvaccinated, primary immunocompromise, pre-existing illness (e.g. HIV, measles), malnutrition
Environmental: smoke, air pollution, mold, crowded housing
Recent hospitalization or antibiotic-use
Physiological: neonates, low-birth weight, underlying lung disease
These factors make the host more susceptible to infection
Infection and proliferation of pathogen in lower respiratory tract/parenchyma
Pediatric pneumonia:
Inflammatory response to infection/proliferation of microbial pathogens at the alveolar level
Exposure to pathogen via inhalation, hematogenous, direct exposure, or aspiration
Epithelial cells in respiratory tract release cytokines that recruit neutrophils & plasma proteins to infection site, initiating a local inflammatory response
Cytokines released into the bloodstream (e.g. TNF, IL-1) initiate a systemic inflammatory response
↑ Vascular permeability
Accumulation of exudate, cellular debris, serous fluid, fibrin, or bacteria in the airway spaces
↑ Respiratory drive
Tachypnea
↑ Excitability of the peripheral somatosensory system
Circulating cytokines induce prostaglandin synthesis
Airway irritation as cilia are unable to efficiently clear fluid buildup
Crackles, ↓ breath sounds
Fluid, protein, or inflammatory cells leak into pleural space
Pleural effusion
Pulmonary edema
Fluid buildup in interstitial spaces ↑ gas diffusion distance
Bacteria enter the bloodstream (if bacterial pneumonia)
Sepsis
Fluid buildup in the alveoli ↓ available surface area for gas diffusion
↓ Efficiency of gas exchange
Intra- and extracranial arteries dilate
Headache
↑ Thermo-regulatory set-point of the hypothalamus
Fever
Myalgia
Hypoxemia
Malaise
Cough
Fluid accumulation in the pleural space prevents full lung expansion
↑ Work of breathing (tracheal tug, paradoxical abdominal breathing, subcostal/suprasternal indrawing)
Legend:
Pathophysiology
Mechanism
Sign/Symptom/Lab Finding
Complications
Published May 28, 2018; updated Aug 25, 2024 on www.thecalgaryguide.com
Pediatric Pneumonia: Pathogenesis and clinical findings
Authors: Jasmine Nguyen Nicola Adderley Reviewers: Midas (Kening) Kang Usama Malik Annie Pham Eric Leung* * MD at time of publication
Immunological: unvaccinated, primary immunocompromise, pre-existing illness (e.g. HIV, measles), malnutrition
Environmental: smoke, air pollution, mold, crowded housing
Recent Hospitalization: length of stay, recent antibiotics, mechanical ventilation
Physiological: neonates, low-birth weight, underlying lung disease (ciliary dysfunction, asthma, cystic fibrosis, bronchiectasis)
Host is more susceptible to infection
Exposure to pathogen:
inhalation, hematogenous, direct, aspiration
Infection and proliferation of pathogen in lower respiratory tract/parenchyma
Pediatric pneumonia:
Inflammatory response to infection/proliferation of microbial pathogens at the alveolar level
Notes:
• Additional findings in pediatric pneumonia may include increased
irritability, nausea/vomiting, diarrhea,
otitis, and headache
• Viral pathogens most common in
children <2yrs; bacterial pathogens most common in children >2yrs
Local inflammatory response: epithelial cells release cytokines in response to infection, which recruit neutrophils and plasma proteins to site of infection
↑ Vascular permeability causes accumulation of plasma exudate, cellular debris, serous fluid, fibrin, or bacteria in the airway spaces
Systemic inflammatory response:
Cytokine release (eg. TNF, IL-1)
↑ respiratory drive
Airway irritation as cilia are unable to efficiently clear fluid buildup
Crackles, ↓ breath sounds
Fluid, protein, or inflammatory
cells leak into pleural space
Pleural effusion
Pulmonary edema
Fluid buildup in interstitial spaces increases gas diffusion distance
Fluid buildup in the alveoli decreases
available surface area for gas diffusion
↓ efficiency of gas exchange
Bacteria invade into the bloodstream (if bacterial pneumonia)
Sepsis
Hypoxemia
Circulating cytokines induce prostaglandin synthesis, which raise the thermoregulatory set-point of the hypothalamus
paradoxical abdominal breathing, subcostal/suprasternal indrawing)
Fever
Cough
Fluid accumulation in the pleural space prevents full
lung expansion, resulting in ↓ lung volumes
Tachypnea
↑ Work of breathing (tracheal tug,
Legend:
Pathophysiology
Mechanism
Sign/Symptom/Lab Finding
Complications
Published Month Day, Year on www.thecalgaryguide.com
Pediatric Pneumonia: Pathogenesis and clinical findings
Immunological: immunization status, immune compromise
Environmental: second-hand smoke, air pollution
Hospitalization: length of stay, recent antibiotics, mechanical ventilation
Neonates, immunocompromise, underlying lung disease (ciliary dysfunction, Cystic Fibrosis, bronchiectasis)
Authors: Nicola Adderley Reviewers: Midas (Kening) Kang Usama Malik Eric Leung* * MD at time of publication
Additional findings in pediatric pneumonia may include nausea, otitis, headache
Viral pathogens most common in children <2yrs; bacterial pathogens most common in children >2yrs
Interstitial pattern: suspect Mycoplasma pneumoniae, Influenza A + B, Parainfluenza Lobar pattern: suspect S. pneumonia, H. influenzae, Moraxella, S. aureus
Systemic inflammatory response:
Cytokine release (eg. TNF, IL-1)
Exposure to pathogen: inhalation, hematogenous, direct, aspiration
Susceptible host and/or virulent pathogen
Infection and proliferation of pathogen in lower respiratory tract/parenchyma
Pediatric pneumonia:
Inflammatory response to proliferation of microbial pathogens at the alveolar level
Notes:
• •
• •
Local inflammatory response: neutrophils recruited to site of infection (LOBAR or INTERSTITIAL PATTERN, depending on pathogen) by epithelial cytokine release
Irritation of contiguous structures and/or referred pain (mechanism unclear)
Acute abdominal pain
Cough
Accumulation of plasma exudate (from capillary leakage at sites of inflammation), cell-debris, serous fluid, bacteria, fibrin
↑ respiratory drive
Disruption of hypothalamic thermoregulation
Fever/chills
Irritation of airways and failure of ciliary clearance to keep up with fluid buildup
Crackles, ↓ breath sounds
Fluid buildup in spaces between
alveoli (INTERSTITIAL PATTERN)
Interstitial opacity on CXR
Fluid buildup in alveoli (LOBAR PATTERN)
↓ efficiency of gas exchange (↑ diffusion distance in INTERSTITIAL, ↓ surface area in LOBAR)
Hypoxemia
Tachypnea
Lobar consolidation on CXR
Respiratory accessory muscle use (chest indrawing, paradoxical breathing, muscle retractions)
Legend:
Pathophysiology
Mechanism
Sign/Symptom/Lab Finding
Complications
Published May 28, 2018 on www.thecalgaryguide.com
gin
Pediatric Pneumonia: Pathogenesis and clinical findings
Authors: Jasmine Nguyen Nicola Adderley Reviewers: Midas (Kening) Kang Usama Malik Annie Pham Eric Leung* Jean Mah* * MD at time of publication
Immunological: unvaccinated, primary immunocompromise, pre-existing illness (e.g. HIV, measles), malnutrition
Environmental: smoke, air pollution, mold, crowded housing
Recent hospitalization or antibiotic-use
Physiological: neonates, low-birth weight, underlying lung disease
These factors make the host more susceptible to infection
Infection and proliferation of pathogen in lower respiratory tract/parenchyma
Pediatric pneumonia:
Inflammatory response to infection/proliferation of microbial pathogens at the alveolar level
Exposure to pathogen via inhalation, hematogenous, direct exposure, or aspiration
Epithelial cells in respiratory tract release cytokines that recruit neutrophils & plasma proteins to infection site, initiating a local inflammatory response
Cytokines released into the bloodstream (e.g. TNF, IL-1) initiate a systemic inflammatory response
↑ Vascular permeability
Accumulation of exudate, cellular debris, serous fluid, fibrin, or bacteria in the airway spaces
↑ Respiratory drive
Tachypnea
↑ Excitability of the peripheral somatosensory system
Circulating cytokines induce prostaglandin synthesis
Airway irritation as cilia are unable to efficiently clear fluid buildup
Crackles, ↓ breath sounds
Fluid, protein, or inflammatory cells leak into pleural space
Pleural effusion
Pulmonary edema
Fluid buildup in interstitial spaces ↑ gas diffusion distance
Bacteria enter the bloodstream (if bacterial pneumonia)
Sepsis
Fluid buildup in the alveoli ↓ available surface area for gas diffusion
↓ Efficiency of gas exchange
Intra- and extracranial arteries dilate
Headache
↑ Thermo-regulatory set-point of the hypothalamus
Fever
Myalgia
Hypoxemia
Malaise
Cough
Fluid accumulation in the pleural space prevents full lung expansion
↑ Work of breathing (tracheal tug, paradoxical abdominal breathing, subcostal/suprasternal indrawing)
Legend:
Pathophysiology
Mechanism
Sign/Symptom/Lab Finding
Complications
Published May 28, 2018; updated Aug 25, 2024 on www.thecalgaryguide.com
Pediatric Pneumonia: Pathogenesis and clinical findings
Authors: Jasmine Nguyen Nicola Adderley Reviewers: Midas (Kening) Kang Usama Malik Annie Pham Eric Leung* * MD at time of publication
Immunological: unvaccinated, primary immunocompromise, pre-existing illness (e.g. HIV, measles), malnutrition
Environmental: smoke, air pollution, mold, crowded housing
Recent Hospitalization: length of stay, recent antibiotics, mechanical ventilation
Physiological: neonates, low-birth weight, underlying lung disease (ciliary dysfunction, asthma, cystic fibrosis, bronchiectasis)
Host is more susceptible to infection
Exposure to pathogen:
inhalation, hematogenous, direct, aspiration
Infection and proliferation of pathogen in lower respiratory tract/parenchyma
Pediatric pneumonia:
Inflammatory response to infection/proliferation of microbial pathogens at the alveolar level
Notes:
• Additional findings in pediatric pneumonia may include increased
irritability, nausea/vomiting, diarrhea,
otitis, and headache
• Viral pathogens most common in
children <2yrs; bacterial pathogens most common in children >2yrs
Local inflammatory response: epithelial cells release cytokines in response to infection, which recruit neutrophils and plasma proteins to site of infection
↑ Vascular permeability causes accumulation of plasma exudate, cellular debris, serous fluid, fibrin, or bacteria in the airway spaces
Systemic inflammatory response:
Cytokine release (eg. TNF, IL-1)
↑ respiratory drive
Airway irritation as cilia are unable to efficiently clear fluid buildup
Crackles, ↓ breath sounds
Fluid, protein, or inflammatory
cells leak into pleural space
Pleural effusion
Pulmonary edema
Fluid buildup in interstitial spaces increases gas diffusion distance
Fluid buildup in the alveoli decreases
available surface area for gas diffusion
↓ efficiency of gas exchange
Bacteria invade into the bloodstream (if bacterial pneumonia)
Sepsis
Hypoxemia
Circulating cytokines induce prostaglandin synthesis, which raise the thermoregulatory set-point of the hypothalamus
paradoxical abdominal breathing, subcostal/suprasternal indrawing)
Fever
Cough
Fluid accumulation in the pleural space prevents full
lung expansion, resulting in ↓ lung volumes
Tachypnea
↑ Work of breathing (tracheal tug,
Legend:
Pathophysiology
Mechanism
Sign/Symptom/Lab Finding
Complications
Published Month Day, Year on www.thecalgaryguide.com
Pediatric Pneumonia: Pathogenesis and clinical findings
Immunological: immunization status, immune compromise
Environmental: second-hand smoke, air pollution
Hospitalization: length of stay, recent antibiotics, mechanical ventilation
Neonates, immunocompromise, underlying lung disease (ciliary dysfunction, Cystic Fibrosis, bronchiectasis)
Authors: Nicola Adderley Reviewers: Midas (Kening) Kang Usama Malik Eric Leung* * MD at time of publication
Additional findings in pediatric pneumonia may include nausea, otitis, headache
Viral pathogens most common in children <2yrs; bacterial pathogens most common in children >2yrs
Interstitial pattern: suspect Mycoplasma pneumoniae, Influenza A + B, Parainfluenza Lobar pattern: suspect S. pneumonia, H. influenzae, Moraxella, S. aureus
Systemic inflammatory response:
Cytokine release (eg. TNF, IL-1)
Exposure to pathogen: inhalation, hematogenous, direct, aspiration
Susceptible host and/or virulent pathogen
Infection and proliferation of pathogen in lower respiratory tract/parenchyma
Pediatric pneumonia:
Inflammatory response to proliferation of microbial pathogens at the alveolar level
Notes:
• •
• •
Local inflammatory response: neutrophils recruited to site of infection (LOBAR or INTERSTITIAL PATTERN, depending on pathogen) by epithelial cytokine release
Irritation of contiguous structures and/or referred pain (mechanism unclear)
Acute abdominal pain
Cough
Accumulation of plasma exudate (from capillary leakage at sites of inflammation), cell-debris, serous fluid, bacteria, fibrin
↑ respiratory drive
Disruption of hypothalamic thermoregulation
Fever/chills
Irritation of airways and failure of ciliary clearance to keep up with fluid buildup
Crackles, ↓ breath sounds
Fluid buildup in spaces between
alveoli (INTERSTITIAL PATTERN)
Interstitial opacity on CXR
Fluid buildup in alveoli (LOBAR PATTERN)
↓ efficiency of gas exchange (↑ diffusion distance in INTERSTITIAL, ↓ surface area in LOBAR)
Hypoxemia
Tachypnea
Lobar consolidation on CXR
Respiratory accessory muscle use (chest indrawing, paradoxical breathing, muscle retractions)
Legend:
Pathophysiology
Mechanism
Sign/Symptom/Lab Finding
Complications
Published May 28, 2018 on www.thecalgaryguide.com
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