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WEEK 18:

Lung pathology- Pneumonia and TB:

QuestionAnswer
pneumonia inflammatory reaction of alveoli and interstitium of the lung caused by an infectious agent
pneumonia characterised by (3) inflammatory exudate in alveolar space that consolidates, inflammation of alveolar septa, and features of acute inflammation
how does pneumonia differ from bronchitis bronchitis is the invasive infection of lower respiratory system (bronchi) but pneumonia is in the alveoli
red hepatization (only in lobar pneumonia) lung becomes firm and red like a liver when neutrophils and fluid in alveoli accumulate and capillaries are congested
routes of infection for pneumonia (3) aspiration, inhalation of pathogen, or contamination from systemic circulation
classification of pneumonia (3) pathogen, setting, or anatomically
lobar pneumonia (alveoli-alveoli) in poor health adults/alcoholic where organisms access alveoli and rapidly spread via alveolar pores to adjacent alveoli
types of anatomical classification of pneumonia lobar pneumonia and bronchopneumonia
bronchopneumonia (bronchi-alveoli) in young/ elderly/ immobile people where organisms colonise bronchi and spread to alveoli. Affected areas consolidate locally at first in lobules then eventually whole lobes
clinical classification of pneumonia (7) community acquired, hospital acquired (nosocomial), pneumonia in immunocompromised patients, aspiration pneumonia, chronic pneumonia, and necrotizing pneumonia + lung abscess
typical (acute) community acquired pneumonia causes 90% of lobar pneumonia and is mostly caused by S. pneumoniae
types of community acquired pneumonia (2) typical (acute) and atypical
causative organisms (5) bacteria (gram +/-), viruses, mycoplasma, fungi, and inorganic agents (inhaled dusts or gases)
aspiration pneumonia occurs when gastric contents and oral bacteria are inhaled into the lungs due to abnormal gag/swallow reflexes
possible outcomes of pneumonia (6) resolution, organisation, abscess formation, empyema, bacteremia, and death
symptoms of all pneumonia (6) fever, chills, dyspnoea, cough with purulent sputum, crackles on auscultation, and consolidation in radiograph
what is used to diagnosis pneumonia (3) sputum is tested (cultured and gram stained to show gram +/-, shape), xray shows symptoms, FBC test to count WBC
treatment for all pneumonia antibiotics
difference between bronchial and vesicular (normal) breathing vesicular is heard over whole lung where inhalation is longer than exhalation but bronchial is only over trachea where expiration is longer than inhalation
describe how TB is a localised lesion TB acts in a small area and body makes granulomas (granulomatous inflammation) to block it with/without involvement of lymphomatous
bacteria causing TB mycobacterium tuberculosis
symptoms of TB (6) gradual onset of anorexia, weight loss, fever (low grade + remitting), night sweats, chest pain, and prolonged coughing with sputum production
diagnosis of TB sputum analysis and chest x ray
sputum analysis of TB shows (3) slender rods (aerobes), a lot of complex lipids (identified by acid fast stains), and cultures (to check drug susceptibility)
pathogenesis of TB in first 3 weeks macrophages engulf inhaled mycobacteria but TB manipulates endosomes (pH and maturation) so phagosome cannot fuse with lysosomes to kill TB so TB survives multiplies inside macrophages
Ghon focus in TB subpleural caseous granuloma (body's attempt to block off bacteria)
Ghon complex in TB ghon focus + lymph node
primary TB (exogenous) ghon focus + ghon complex formed as a fibrous encapsulation to block off infection making TB latent (dormant) but TB survives well leading to hypersensitivity of host (tissue damage) with patients having little/no symptoms
secondary TB (reactivated) occurs if patient is weak/ immunocompromised where TB is reactivated meaning caseating tubercle enlarges and erodes into bronchial wall/ vessels leading to live microbes in sputum
re-exposure of TB spreads through which vessel (systemic dissemination) pulmonary vein
cavitation caseating tubercle (lesion) erodes into lung vasculature
obstructive diseases of airway + gas exchange (5) asthma, chronic bronchitis, emphysema, bronchiectasis, and cystic fibrosis
restrictive diseases of airway + gas exchange (4) ARDS, pulmonary fibroses, pneumoconioses (asbestosis/ silicosis), and granulomatous disease (sarcoidosis)
pulmonary infections (2) pneumonia and TB
upper airway diseases (2) nasopharyngeal carcinoma and laryngeal tumours
vascular diseases (4) pulmonary hypertension, pulmonary embolism, haemorrhage, and infarction
neoplasm (abnormal cell growth) disease lung cancer
pleural disease (3) pleurisy, pneumothorax, and cancer
atelectasis collapse of one or more lobes of lung
organisation exudate is converted into fibromyxoid masses by macrophages and fibroblasts
what can cause reflexes protecting airways to fail leading to aspiration pneumonia stroke, unconsciousness, repeated vomiting, and underlying disease (MS)
what happens in aspiration pneumonia often necrotising leading to death but survivors form abscess
abscess full of pus
pathogenesis of TB after 3 weeks cell mediated response occurs where macrophages drain into lymph nodes and present antigens to T cells. T cells become TH1 which release INF-Y and these activate macrophages
granulomas cluster of immune cells
secondary TB in bronchial wall causes tuberculous bronchopneumonia (in lower lobes and rapidly progresses into whole lung - galloping consumption)
secondary TB in vessel causes miliary or isolated organ TB
what causes miliary TB in lungs TB spread back towards lungs via pulmonary artery via lymphatic drainage into right side of heart
effect of miliary TB in organs grow and merge (coalesce) and destroy large areas of affected organs eg liver/kidney
isolated organ (metastatic) TB few TB bacteria invade bloodstream and reach specific organ (eg brain,/ kidney) where the body either contains them or they remain latent for years
dysphagia problem swallowing
Created by: kablooey
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