summary Flashcards
IDIOPATHIC PULMONARY FIBROSIS
@
USUAL INTERSTITIAL PNEUMONIA
*medicine m/s 239
Risk factors : men, older age , smoking, antidepressants, chronic aspiration(gastro-esophageal reflux), exposure to toxic dust, fumes, and autoantibodies.
Clinical Features : progressive dyspnoea, dry cough, end-inspiratory crackles, clubbing, which eventually lead to cyanosis, respiratory failure,pulmonary hypertension and cor pulmonale.
investigation : lung biopsy shows heterogenous appearance, alternating areas of normal lung, interstitial inflammation, fibrosis and honey-combing.(more severe subpleurally). High-resolution CT scan typically shows evidence of advanced fibrosis, with extensive areas of reticulation and honey-combing with minimal ground-glass opacities.
treatment : respond poorly on corticosteroid. high mortality
SARCOIDOSIS
- medicine m/s 244
Sarcoidosis is a multisystem, chronic granulomatous inflammatory disorder, unknown aetiology. characterised by the accumulation of T lymphocytes and mononuclear phagocytes and non-caseating epithelioid granulomas in the affected organs.
~can be pulmonary/extrapulmonary
investigation : accumulation CD4 cell with compartmentalisation in affected tissues associated with corresponding depletion of CD4 cells in other tissues and depression of some delayed-type hypersensitivity responses, thus patients demonstrate with negative reactions to tuberculin test.
Acute (transient& resolve spontaneously): young adult + erythema nodosum + bilateral hilar lymphadenopathy + arthritis + uveitis
Chronic (persistent): older age + progressive lung fibrosis + extrapulmonnary sarcoidosis
HYPERSENSITIVITY PNEUMONITIS
- respi textbook m/s 147
typical example : farmer’s lung &bird fancier’s lung
provoking Ag : fungal spore, avian Ag
immunologically mediated lung disease which hypersensitivity response occurs in an individual sensitised to an inhaled antigen.
pathogenesis : inhale antigens provokes a complex immune response in susceptible individuals, involving antibody reactions, immune-complex formation, complement activation and cellular responses, resulting in alveolitis.
acute form : recurrent episodes of dyspnoea,dry cough, pyrexia, myalgia and a flu-like sensation
chronic form : dyspnoea, lung fibrosis. Lung biopsies show features of fibrosis, alveolitis and granuloma formation. Bronchoalveolar lavage shows lymphocytic alveolitis, predominance of T-suppressor lymphocytes.
Precipitating antibodies to antigens can be detected in serum
treatment : cessation to provoking Ag.
SILICOSIS
*respi textbook m/s 186
due to inhalation silicon dioxide
xray : eggshell calcification of hilar lymph node and upper lobe fibrosis(nodular opacities), pleural thickening
complication : increase risk lung cancer, COPD, increased risk
of tuberculosis as silica interferes with the ability of macrophages to kill tubercle bacilli.
ASBESTOSIS
- respi textbook m/s 188
diffuse lung fibrosis due to prolongation heavy exposure to asbestos. slowly progress even after cessation to asbestos
xray : bilateral, predominantly basal reticulonodular shadowing
ct scan : Fibrosis is usually first evident around the respiratory bronchioles at the lung bases, becoming more diffuse as the
disease progresses
light/electron microscopy : Asbestos bodies(asbestos fibre coated with an iron-containing protein) seen within areas of fibrosis
#not respond to corticosteroid complication : high risk develop lung cancer
COAL WORKER’S PNEUMOCONIOSIS
*respi textbook m/s 185
2 categories : simple & complicated
pathogenesis : Coal dust inhaled into the alveoli is taken up by macrophages, which are then cleared via the lymphatic drainage system or the mucociliary escalator of the bronchial tree. heavy prolonged
exposure to dust, clearance mechanisms overwhelmed and dust macules arise particularly in the respiratory bronchioles. Release of dust from dying macrophages induces fibroblast proliferation and fibrosis
one type of noon-cardiogenic pulmonary oedema
ARDS @ SHOCK LUNG @ DIFFUSE ALVEOLAR DAMAGE
rapid onset life-threatening respiratory distress with cyanosis, severe hypoxemia, acidosis.it not respond to O2 therapy
*medicine m/s 132
pathogenesis : in respond to initiating injury( can be direct/indirect)(direct: gastric content aspiration,severe pneumonia,lung contusion)(indirect: sepsis, pancreatitis,DIC) it cause development inflammatory cascade.macrophage release IL8,IL1,TNF.neutrophil migrates to alveolus get activated and then release factor which cause capillary endothelial and alveolar epithelium injury,edema fluid accumulation within alveoli,hyaline membrane formation and surfactant inactivation. alveolar capillary permeability increase result pukmonary oedema and lead to acute respiratory failure(ARDS)
PULMONARY EDEMA
= leakage of interstitial fluid which accumulate in alveolar space
macroscopy: frothy fluid congested lung
microscopy: thickened alveolar wall, dilated capillary, interstitial edema, transudate in alveolar lumen(pale pink)
cardiogenic pulmonary edema/ hemodynamic pulmonary cause : increase hydrostatic pressure, left sidex heart failure, volume overload, renal failure, nephrotic syndrome, hypoalbuneamia
microvascular injury cause : sama mcm ARDS punya cause
hemodynamic pulmonary edema: fluid accumulates at basal region lower lobe sbb greater hydrostatic pressure. microscopically ada hemosiderin-laden macrophage( heart-failure cell)
microvascular injury: injury to capillay of alveolar septa to takde increase in hydrostatic pressure. sama cam pathogenesis ARDS
CF : dyspnea, tachypnea, hypercapnia, cyanosis, frothy& blood-tinged sputum, crepitation at lung base
PULMONARY EMBOLISM
most of emboli are thrombo(blood clot). 95% from deep vein thrombosis
*respi textbook m/s 195
cardinal features: dyspnea,tachypnea >20/min, pleuritic pain
risk factor: virchow’s triad ( stasis, endothelial injury, hypercoagulability); prolong immobilization, CHF, knee/hip surgery, burns/multiple fracture, OCP with high est, factor V Leiden gene
mutation, antithrombin III, protein S or protein C deficiencies
CF: calf pain, unilateral swelling, redness, hemoptysis, dyspnea, chest pain, reduce breath sound
complication: pulmonary hpt, acute r heart failure, pulmonary infarction
normal : pulmonary arterial pressure is about 20/8 mmHg and the mean pulmonary artery pressure is 12–15 mmHg.
PULMONARY HYPERTENSION
= mean pulmonary artery pressure >25 mmHg at rest
cause : hypoxaemia and chronic lung disease( cor pulmonale) but in some cases can be idiopathic
pulmonary hypertension.
CF : exertional dyspnea, angina, syncope, peripheral edema, jugular venous distension
COR PULMONALE
development of pulmonary hypertension and right ventricular hypertrophy secondary to disease of the lungs
causes :
1. Hypoxaemia
2. vascular obstruction (e.g. chronic pulmonary emboli,
pulmonary artery stenosis),
3. increased blood flow
(e.g. left-to-right intracardiac shunts – atrial and ventricular septal defects)
4. loss of pulmonary vascular bed (e.g. fibrotic lung disease,emphysema)
5. increase blood viscosity eg:polycythemia vera, sickle cell,macroglobulinemia
6. primary pulmonary hpt
CF : elevation of jugular venous pressure, hepatomegaly(as a result of congestion), peripheral oedema,
a prominent left parasternal heave, a loud pulmonary secondary sound, chest X-ray may show large pulmonary arteries with pruning
PNEUMONIA
- CAP
- CAAP
- HAP/VAP/NOSOCOMIAL PNEUMONIA
- CHRONIC PNEUMONIA/PULMONARY TB
- ASPIRATION PNEUMONIA
- NECROTIZING PNEUMONIA/LUNG ABSCESS
- IMMUNOCOMPROMISED PNEUMONIA
bacteria pneumonia has 2 anatomical distribution: bronchopneumonia/lobar pneumonia
*syamin note/medicine m/s 143
STAGES OF INFLAMMATORY RESPOND IN LOBAR PNEUMONIA:
- congestion: the lungs are filled with fluid due to the inflammatory process and the leaky blood vessels cause a massive collection of fluid in the lungs. heavy&boggy affected lobe
- red hepatisation: now that the congestion resolves to some extent, the lung now becomes firm&airless with liver-like consistency. red in appearance due alveolar space packed with neutrophil,red cell&fibrin.
- grey hepatisation: lung firm,dry&gray due to red cell lyses. fibrinosuppirative exudate remain in alveolar space.
- resolution: exudate being digested by enzyme then being ingested by macrophage and organized by fibroblast
COMPLICATION:
ARDS,pneumothorax, lung abscess,empyema,septicemia
(1) tissue destruction
and necrosis, causing abscess formation;(2) spread of infection
to the pleural cavity, causing the intrapleural fibrinosuppurative
reaction known as empyema; and (3) bacteremic dissemina-
tion to the heart valves, pericardium, brain, kidneys, spleen, or
joints, causing metastatic abscesses, endocarditis, meningitis, or
suppurative arthritis.
- pneumonia can be contagious/non-contagious.compare to TB it is contagious via respiratory droplet(cough/sneeze). for pneumonia if immunocompetent, person just develop mild respi tract infection.it is rare unless immunocompromised.
TUBERCULOSIS
q
PULMONARY EDEMA VS PNEUMONIA
- Pneumonia is bacterial or viral in origin. Pulmonary edema is usually due to systemic pathology or volume overload in heart failure.
- Pneumonia presents very early and causes severe respiratory distress earlier. Pulmonary edema presents later and most often in elderly and in heart failure patients
- Pneumonia can be acquired in the community or hospitals. Pulmonary edema usually does not occur acutely
BOTH present with
respiratory distress, dyspnea, exertion and fatigue, cyanosis
**Pneumonia can cause pulmonary edema as the inflammatory state in pneumonia can cause leakage of fluid from the blood vessels and capillaries thus causing massive collection of fluid in the lungs that give an appearance like that of pulmonary edema.
LUNG ABSCESS
= localized area of suppurative necrosis within the pulmonary parenchyma, resulting in
the formation of one or more large cavities.
causative organism may be introduced into the lung by:
• Aspiration of infective material from carious teeth or infected sinuses or tonsils. This may occur during oral
surgery, anesthesia, coma, or alcoholic intoxication, and
in debilitated patients with depressed cough reflexes.
• Aspiration of gastric contents,
• As a complication of necrotizing bacterial pneumonias, particularly those caused by S. aureus, Streptococcus pyogenes, K. pneumoniae, Pseudomonas spp.
• Bronchial obstruction
• Septic embolism, from infective endocarditis of the right
side of the heart.
• hematogenous spread of bacteria in disseminated pyogenic
infection. staphylococcal bacteremia and often results in multiple lung
abscesses.
Anaerobic bacteria are present in almost all lung
The most frequently encountered anaerobes normally found in the oral cavity; Prevotella, Fusobacterium, Bacteroides, Peptostreptococcus, and microaerophilic streptococci.
more common on the right side (with its more vertical airways) than on the left, and most are single. On the right side,they tend to be in the posterior segment of the upper lobe
and in the apical segments of the lower lobe. Abscesses that develop in the course of pneumonia or bronchiectasis commonly are multiple, basal,and diffusely scattered. Septic emboli and abscesses arising from
hematogenous seeding are commonly multiple at any region of the lungs.
complication: abscess rupture form air-fluid level on radiographic exami-
nation, pneumothorax or empyema, emboli to brain cause meningitis or brain abscess.
Clinical Features:foul-smelling, purulent sputum, hemoptysis, Spiking fever, malaise, Clubbing
