L13 Pneumonia and Bronchiectasis Flashcards
Classification of Pneumonia?
Pneumonia is an inflammatory process of the lung c aused by an infectious agent: (bacterial, viral or fungal)
(1) Clinical circumstances
- Community acquired (typical/atypical)
- Hospital acquired (nosocomial)
- Opportunistic
(2) Etiological agent
- Bacterial
- Viral
- Fungal
- Other
(3) Anatomical pattern
Bronchopneumonia
Characteristics?
Demographics?
Micro-characteristics?
Bronchopneumonia
- Patchy consolidated areas of acute suppurative (pus) inflammation
- Centered on bronchioles and bronchi - Often multilobar and bilateral
- Infancy and old age
- Arises from chronic debilitating illness
- Neutrophil-rich exudate, fills the bronchi, bronchioles and alveola
Lobar Pneumonia
Characteristics
Demographics
Cause?
Stages?
Lobar Pneumonia
Affects a large part of lobe or entire lobe
Typically affects otherwise healthy adults
Rarer now w/ antibiotics
Strep. Pneumoniae (90%)
Stages:
1. Congestion
2. Red Hepatization
3. Gray Hepatization
4. Resolution
Stages of Lobar Pneumonia?
1. Congestion
- Vascular engorgement
- Intra-alveolar proteinaceous fluid
- numerous bacteria in alveoli
- Lung heavy, boggy, red
2. Red Hepatization
- Massive congestion of lung parenchyma
- Neutrophils and fibrin fill alveolar spaces
- Lung appears red, firm, airless, liver-like
3. Gray Hepatization
- Disintegration of RBCs
- Fibrosuppurative exudate
- Gray/brown, dry surface
4. Resolution
- Occurs at 8-10 days
- Enzymatic digestion of consolidated exudate
- Produces semisolid debris
- Resorbed
- Ingested by macrophages
- Coughed up
- Produces semisolid debris
- Pleural fibrinous reaction may similarly resolve or undergo organization leaving permanent fibrous adhesions
Host Pneumonia Defence Mechanisms?
When does pneumonia infection occur?
Infection results when:
- Defect in host immunity (intrinsic factor)
- Particularly virulent organism (extrinsic)
- Evasion of muco-ciliary clearance
- Evasion of macrophage-induced killing
- Overwhelming inoculum of infecting organism (extrinsic)
Predisposing Host Factors for Pneumonia (7)
• Loss of cough reflex
– Neuromuscular disorders
– Cerebrovascular accident
– Coma
• Damage to muco-ciliary apparatus
– Smoking
– Kartagener syndrome
– I_mmotile cilia syndrome_
• Accumulation of secretions
– COPD
– Bronchiectasis (CF)
• Pulmonary congestion and oedema
• Decreased alveolar macrophage function
– Alcohol
– Smoking
• Drugs
– Immunosuppressants
– H2 antagonists
• Bronchial obstruction
– Bronchogenic carcinoma
– Foreign body
__________: Chronic necrotizing infection of the bronchi and bronchioles
=> associated with ___________________ of these airways
Bronchiectasis: Chronic necrotizing infection of the bronchi and bronchioles
=> associated with abnormal, irreversible dilation of these airways
Weakening/dilatation of lumen of airway => once dilated, does not return to normal
Airways are dilated, up to 4x normal diameter and filled with pus
Bronchietasis is a secondary diesase due to?
It is a secondary disease, due to
(1) Obstruction
(2) Persistent severe infection
What part of the lung is usually affected by bronchiectasis?
Typically affects Lower Lobes Bilaterally
Pathophysiology of Bronchiectasis (5 Steps)
2 main requirements:
– Impaired drainage, airway obstruction or defect in host defense
– Infectious insult
Clinical Features of Bronchiectasis
Clinical Features:
Symptoms:
- Severe persistent cough
- Production of large volumes of mucopurulent sputum
Signs:
- Crepitations
- Wheeze
- Clubbing of the fingers
- Cor pulmonale (right ventricular failure)
Investigations of Bronchiectasis?
Investigations
Blood tests (Not diagnostic) – Raised WCC and CRP if infective exacerbation
Radiology– CXR/CT thorax
Microbiology– Sputum C+S (Pseudomonas sp)
What causes cystic fibrosis?
Multi-system disease caused by a(recessive) genetic mutation in the gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR) protein on Chr. 7q31
=>Thick, viscous secretions in lungs, pancreas, liver, intestine, reproductive tract
Presentation of cystic fibrosis in Adults vs. Children?
Presentation in infancy:
–Common mutations in CFTR gene
–Meconium ileus (blockage of the small intestine)
–Respiratory symptoms
–Failure to thrive
Presentation in adulthood
–Rare mutations in CFTR gene
–Gastrointestinal symptoms
–Diabetes mellitus
–infertility
Main cause of mortality from cystic fibrosis?
Respiratory Disease main cause of mortality (Bronchiectasis, Chronic Bronchitis)
Primary causative organisms of Cystic Fibrosis
Infection w/
Pseudomonas aeruginosa
Burkholderia cepacia complex
Screening for Cystic Fibrosis?
Screening
Newborn Heel prick test
DNA analysis
Sweat Chloride Test
Nasal potential differences– Abnormalities in epithelial chloride secretion
Treatment of Cystic Fibrosis (Respiratory/GI)
Respiratory:
– Antibiotics
– Physiotherapy
– Bronchodilators
– Oxygen
– CFTR potentiators/correctors
Ataluren
permits selective ribosomal read-through of the premature termination codon
=> allows production of full length transcript and CFTR protein.
Lumacaftor
Interacts w/ the CFTR to facilitate its correct folding
=> allow proper trafficking of CFTR to the cell surface.
Ivacaftor
stabilizes the open state of the CFTR => increases channel opening time
– Transplantation
Gastrointestinal:
– Pancreatic enzyme replacement therapy (PERT)
– Fat-soluble vitamin supplementation
_______________: permits selective ribosomal read-through of the premature termination codon
=> allows production of full length transcript and CFTR protein.
Ataluren: permits selective ribosomal read-through of the premature termination codon
=> allows production of full length transcript and CFTR protein.
_______________: Interacts w/ the CFTR to facilitate its correct folding
=> allow proper trafficking of CFTR to the cell surface.
Lumacaftor: Interacts w/ the CFTR to facilitate its correct folding
=> allow proper trafficking of CFTR to the cell surface.
______________: stabilizes the open state of the CFTR
=> increases channel opening time
Ivacaftor: stabilizes the open state of the CFTR => increases channel opening time
