respi patho Flashcards
defences against infection in lungs (3)
- large microbes trapped in mucus -> transported to throat by ciliary action -> swallowed
- cough reflex
- smaller organisms phagocytosed by alveolar macrophage/if enter bloodstream, will incite immune response
which parts of the aiway is sterile
- anywhere below the vocal chords (ie LOWER RESPIRATORY TRACT) -> due to defence mechanisms
main causative organism of acute URTI
viral infection
pathology of rhinitis (2)
INFECTIVE (mostly viral) -> surface epithelial cells necrosis -> exudation of fluid and mucous and swelling -> nasal obstruction
ALLERGIC -> hypersensitive to environmental agent, mast cell degranulation etc -> produce exudate and mucosal edema -> if antigenic stimulus persists, mucosa becomes swollen and polypoid -> formation of nasal polyps
which parts of the sinus is affected in sinusitis
- inflammation of the paranasal sinus linings of ANTERIOR GROUP of sinuses (maxillary, ethmoid and frontal sinuses)
complication of sinusitis
- mucosal edema (edema build up in mucosa forming a small lump) -> impair drainage of secretion -> secondary bacterial infection
clinical presentation of acute laryngitis and pharyngitis (3)
- sore throat (supraglottic)
- hoarseness (glottic)
- cough and tracheal soreness (subglottic)
acute laryngitis and pharyngitis is usually caused by:
viral infection
why is acute laryngitis and pharyngitis dangerous in young children
- children have small airways that are easy to collapse, mucosal & submucosal edema can cause airway obstruction easily
describe breathing sound in children with acute pharyngitis/ laryngitis
stridor
stridor + cough = coup
predisposing factor to chronic laryngitis + pathogenesis
- heavy smokers
- chronic irritation of epithelium cause squamous metaplasia
chronic laryngitis increases risk of:
dysplasia and squamous cell carcinoma
most common laryngeal carcinoma & location
SQUAMOUS CELL CARCINOMA (95%)
- mostly GLOTTIC (can be supraglottic/ subglottic)
risk factors for squamous cell carcinoma of LARYNX
- Smoking (alw associated with SCC)
- Alcoholism
- Asbestos
- Chronic laryngitis
describe benign lesions of the larynx (2)
- singer’s nodules -> stress vocal chords too much; cause HOARSENESS
- laryngeal papilloma/ squamous papilloma -> due to HPV INFECTION
patient presents with facial edema and bronchospasm
allergic pharyngolaryngeal edema
- life threatening Type I hypersensitivity
types of nasopharyngeal carcinoma (3)
- keratinizing NPC
- differentiated nonkeratinizing NPC
- UNDIFFERENTIATED NONKERATINIZING NPC (most common!!! 95% of NPCs)
main risk factors for keratinizing NPC (nasopharyngeal carcinoma) (2)
- EBV INFECTION (at nasopharyngeal epithelium) at young age -> presents as infectious mononucleosis
- family history -> esp SOUTHERN CHINESE
NPC clinical presentations
- hearing loss, tinnitus
- diplopia
- nasal obstruction
- cervical lymph node metastasis
what tests are recommended for people with fam history of NPC? (2)
- EBV IgA antibody -> IgA usually precedes tumour development by a few years
- nasoendoscopy
inhaling hot toxic fumes in a fire cause:
acute toxic laryngitis
three types of atelectasis and their causes (3)
- Resorption -> obstruction of alveoli, O2 in alveoli resorbed thus alveoli collapses
- Compression -> by pleural effusion/ haemothorax/ pneumothorax
- Contraction -> lung fibrosis cause loss of surfactant -> alveoli collapse
what does atelectasis predispose a patient to
- INFECTION due to mucus trapping
- and hypoxia
bronchiolitis pathogenesis
- inflammation of airway diameter <2mm (BRONCHIOLES)
- macrophage infiltrate airways, cause SCARRING & NARROWING -> obstruction of airway
bronchitis vs bronchiolitis (2)
- difference in region infected (bronchi vs bronchiole)
- bronchitis have MUCUS production (hyperplasia of mucus glands are seen in CHRONIC bronchitis)
causative organism for bronchitis/ bronchiolitis
VIRUSES
- eg influenza tracheobronchitis, respiratory syncitial virus (RSV) bronchiolitis
broncho pneumonia pathogenesis & complications
- bronchi infected -> spread to bronchioles & alveoli
complication: lung abscess
lobar pneumonia pathogenesis & complications
- Organisms begin infection from bronchioles & alveolar space (does not start from bronchi)
complication: bacteremia
common organism in lobar pneumonia
S pneumonia, Klebsiella
aspiration pneumonia pathogenesis & complication
- swelling or aninfectionof the lungs/ large airwaysdue tounconscious/ impaired swallowing
complication: lung abscess
aspiration pneumonia causative organisms
causative organisms: oropharyngeal bacteria, anaerobes
IMAGING: pneumonia
- basically opaque white block (usually at bottom of lung), no pulmonary vessels
- differentiate from pleural effusion: pneumonia still HAS costophrenic angle
- differentiate from mass: pneumonia has poorly defined margins
what is lung abscess
localized area of suppurative necrosis, usually forming large cavities
what causes lung abscess (6)
- broncho pneumonia
- aspiration pneumonia
- septic emboli (eg Staph aureus)
- trauma
- bronchiectasis -> bronchial obstruction -> accumulate mucus -> infection & necrosis
- pulmonary infarction -> necrosis
complications of lung abscess (4)
- Empyema (rupture into pleura)
- Bronchopleural fistula
- Haemorrhage from erosion into pulmonary vessel
- Septicaemia
lung abscess vs empyema
- lung abscess involves LUNG PARENCHYMA
- empyema involves PLEURAL SPACE
lung abscess contains mainly?
neutrophils
atypical pneumonia causative organisms
- Mycoplasma (#1), legionella, chlamydia, rickettsia
IMAGING & presentation: atypical pneumonia
- absence of consolidation on Xray due to minimal airspace exudate
- interstitial inflammation (pneumonitis) thus increase interstitial markings in Xray
presentation:
- symptoms of pneumonia
what type of hypersensitivity is hypersensitivity pneumonitis
- Acute exposure –> type III hyper sensitivity response –> respiratory 4-8 hours after exposure
- Repeated exposure -> sensitisation and type IV hypersensitivity reaction –> insidious development of dyspnoea and pulmonary fibrosis in a patient that has not experienced acute symptoms
IMAGING: pneumonitis
pneumonitis:
- inflammatory disease dominated by interstitial inflammation -> increase interstitial markings in Xray
TB histo presentations (3)
- Granuloma (epithelioid histiocytes surrounding area of central caseous necrosis)
- Multinucleated giant cells
- Lymphocytes
risk factors for TB
- poverty, crowded, endemic areas
- immunocompromised: diabetes, HIV
- alcoholic
- chronic lung diseases
complications of pri TB (uncommon)
progresses with severe pneumonia & dissemination
- continuing enlargement of the caseating granulomas in the lymph nodes
- spread occurs by the enlarging nodes eroding either
1) through wall of a bronchus (tuberculous bronchopneumonia) 2) into a thin-walled blood vessel (miliary TB)
primary vs secondary TB
- lymph node involvement more evident in pri TB -> secondary TB immune cells immediately activated to contain infection
- secondary TB found at apex of lung in CXR, pri TB at lymph nodes
- secondary TB cause increase tissue destruction (greater immune response)
complications of secondary TB
Vigorous immune response:
healing of apical lesion -> leave central area of caseous necrotic material (may contain bacteria) surrounded by dense collagenous wall -> calcifies (fibrocaseous TB)
* If immune response weakens and still have bacteria -> reactivated fibrocaseous tuberculosis
Poor immune response:
progressive enlargement of apical lesion -> continued destruction of lung tissue
* Bigger lesion -> increase risk of erosion into blood vessels or airways
IMAGING: secondary TB
- TB always found at APEX of lungs (highest pO2)
- little lymph node involvement (granuloma is contained in CXR) as immune system recognises and contains it
IMAGING: miliary TB
- millet seed appearance (many white spots all over lung)
bronchiectasis pathogenesis
permanent abnormal dilation of main bronchi -> cycle of inflammation, mucus secretion, infection, airway dilation/destruction
bronchiectasis clinical presentations (3)
- recurrent infection
- hemoptysis
- mucopurulent sputum production lasting months to years
predisposing factors to bronchiectasis (2)
Drainage secretion obstruction
- cystic fibrosis
- immotile cilia syndrome
Recurrent and persistent infection
complications of bronchiectasis
- cor pulmonale
- lung abscess
- systemic amyloidosis
- pyemia (pus bacteria released into blood) causing brain abscess
obstructive vs restrictive lung disease - differences (4)
FEV1/FVC
- obstructive (<0.7-0.8)
- restrictive (>0.7-0.8)
Lung capacity
- obstructive: normal capacity
- restrictive: lowered capacity
Expiratory flow rate
- obstructive: reduced
- restrictive: normal
Pathogenesis
- obstructive: airway blockage
- restrictive: parenchymal
obstructive lung diseases - causes (3)
- obstructive sleep apnea
- asthma
- COPD
risk factor for OSA (obstructive sleep apnea)
- men, obese
asthma pathogenesis
- triggered by atopic (allergen)/ non atopic agents (non allergen, eg cold)
- affects BRONCHI (mucus produced)
3 immediate effects of asthma on bronchi
- hypertrophy of smooth muscle
- hypersecretion of mucus + mucosal edema
- bronchial mucosa infiltrated with eosinophils, mast cells, lymphoid cells, macrophage
status asthmaticus
acute severe asthma -> cannot be treated by inhalers/steroids, cause respiratory failure
COPD characteristics (3)
- emphysema
- chronic bronchitis -> cough with sputum (mucus hyper secretion) + narrowing of airway
- bronchiolitis -> airway scarring
causes of emphysema (3)
- SMOKING -> inhibit a1-antitrypsin -> protease protease inhibitor imbalance -> protease cause tissue destruction
- CONGENITAL a1-antitrypsin deficiency
- pneumoconiosis
complications of emphysema (3)
- Cor pulmonale
- Respiratory failure
- Pneumothorax
- Peptic ulcer
barrel chest is a sign of:
emphysema
IMAGING: emphysema
- too many posterior ribs visible
- compressed diaphragm on both sides
difference between COPD vs asthma (2)
- COPD is IRREVERSIBLE (bronchospasm/constriction in asthma reversible)
- COPD is PROGRESSIVE (asthma is recurrent acute attacks)
restrictive lung diseases - causes (2)
- interstitial edema
- fibrosis of alveoli (diffuse parenchymal lung disease)
cause of interstitial edema in restrictive lung diseases (1)
acute stage of ARDS (acute respiratory distress syndrome) - fluid accumulation in alveoli due to systemic sepsis/ severe trauma or burn/ inhalation of toxic fume
-> damage to alveolar capillary endothelium OR alveolar lining cell
characteristics of diffuse parenchymal lung disease (4)
- widespread INFLAMMATION in interstitium
- reduced lung COMPLIANCE
- EDEMA and FIBROSIS
- alveolar wall thickening -> reduced gas exchange
main causes of parenchymal lung disease
- IDIOPATHIC (most common)
- late organisation phase of ARDS (2nd most common)
- pneumoconiosis (inhale dust - eg silica/ coal dust/ asbestos)
- end stage pulmonary fibrosis
histological patterns of reaction in lung parenchymal damage (7)
Alveoli
- Haemorrhage
- Fibrin exudation -> form hyaline membrane
- Macrophage accumulation
- Fibrosis
Interstitium:
- Edema
- Inflammation
- Fibrosis
ARDS pathogenesis
acute phase -> fluid accumulation in alveoli and damaged secondary to other reasons
late organisation phase -> regeneration of Type II alveolar lining cells and hyaline membrane with fibrosis + inflammation and fibrosis of interstitium -> HONEYCOMB LUNG -> death by RESPI & CARDIAC failure
predisposing factor to pneumoconiosis
- occupational exposure
- smoking (worsens condition)
forms of lung cancer (2)
- small cell carcinoma (20%)
- non small cell carcinoma (squamous cell carcinoma + adenocarcinoma)
cause of small cell carcinoma + prognosis
- SMOKING
- poor prognosis -> central, rapid growth
main feature of squamous cell carcinoma (1)
central cavitation
main cause of squamous cell carcinoma (1)
- SMOKING
*more common in MALES
is adenocarcinoma related to smoking or gender?
NO, NO (present in both genders equally)
IMAGING: minimally invasive adenocarcinoma (vs other lung carcinoma)
- NO MASS, similar to consolidation as cancer spreads along alveolar septa,
- other lung carcinoma -> mass
how does lung cancer spread (4)
- Local -> lung, pleura, mediastinal structures, chest wall
- Lymphatic -> lymph nodes (mediastinum, neck, others)
- Transcoelomic (across the peritoneal cavity) -> pleural and pericardial effusions
- Haematogenous
paraneoplastic syndromes of lung cancer
- SIADH (syndrome of inappropriate ADH secretion)
- Cushing’s syndrome (Excessive ACTH Secretion, EAS)
- Hypercalcaemia (PTHrp)
pleural diseases (6)
- haemothorax (blood)
- pneumothorax (air)
- pleural effusion (fluid - pus/ edema)
- chylothorax (chyle from thoracic duct)
- pleurisy (pleural inflammation, neutrophils predominate)
- cancer
causes of pneumothorax (3)
- spontaneous (primary [thin young men/ rupture of congenital sub pleural apical bleb] & secondary [rupture of emphysematous bulla/ asthmatics])
- traumatic
- iatrogenic (caused by medical examination)
IMAGING: open/ closed pneumothorax
- smaller lung (wrapped by air) in Xray
- diaphragm depressed
IMAGING: tension pneumothorax
- smaller lung (wrapped by air) in Xray
- diaphragm depressed
- shift in mediastinum position (bilateral tension pneumothorax may not show mediastinum shift)
describe the fluid in pleural effusion (2)
EXUDATE [high protein] - eg empyema (pus in pleura) from pneumonia; haemothorax from rib fracture
TRANSUDATE [low protein] - eg pulmonary edema, HF
IMAGING: pleural effusion
- NO COSTOPHRENIC ANGLE, with meniscus
- opacity at base of lung
what is predominantly found in pleurisy
- pleura inflammation -> neutrophil predominate
types of pleural cancer (2)
- 2ndary metastatic carcinoma (most common)
- malignant mesothelioma (pri tumour) -> due to ASBESTOS exposure
why is lungs/ liver a common site of metastasis from other cancers
- end capillary bed
anterior mediastinum mass likely diagnosis
thymoma
what is thymoma associated with
myasthenia gravis
middle mediastinum mass likely diagnosis
enlarged hilar lymph nodes (due to sacoidosis, lung cancer, TB etc)
posterior mediastinum mass likely diagnosis
schwannoma (nerve sheath tumour)
causes of lung granulomas (4)
- infection (eg TB/ fungal infection)
- foreign matter (pneumoconiosis, hypersensitivity pneumonitis)
- unknown causes (sarcoidosis) -> characterised by nonnecrotising granulomas in many tissues and organs
- wegener’s granulomatosis
predisposing factor of sarcoidosis (race related, my fav disease)
- rare in chinese
- common in caucasians, black, indian
neonatal diseases
- developmental anomalies -> bronchial atresia/ bronchogenic cysts/ bronchopulmonary sequestration
- neonatal respiratory distress syndrome
- immotile cilia syndrome (abnormal cilia structure/ unable to beat coordinately)
- cystic fibrosis
what is bronchial atresia
obstruction of bronchial segment
what is bronchogenic cyst
accessory bronchial buds that become sealed off from airway
what is bronchopulmonary sequestration
lung tissue with blood supply but no respiratory function (not connected to bronchial tree)
neonatal respiratory distress syndrome pathogenesis
- deficiency in lung surfactant (usually premature birth) causing alveolar collapse
**AKA hyaline membrane disease
effects of neonatal respiratory distress syndrome on lungs (3)
- Hypoxia
- Damage to endothelial and alveolar lining cells
- Fibrin exudation (forms hyaline membrane)
cystic fibrosis pathogenesis
- autosomal recessive
- abnormal viscous mucus -> builds up in lungs, pancreas, and other organs
- predispose to repeat infections and BRONCHIECTASIS
lung diseases secondary to systemic diseases/ lung diseases causing systemic disease (5)
- pulmonary edema due to LH failure
- pulmonary arterial hypertension
- cor pulmonale
- pulmonary emboli
- pulmonary vasculitis
causes of pulmonary hypertension (4)
- LH failure
- pulmonary emboli
- L to R shunt (ASD/ VSD/ PFO-patent foramen ovale)
- chronic lung disease (loss of capillaries + hypoxic vasoconstriction of arteries)
consequence of ARTERIAL hypertension
- TUNICA MEDIA hypertrophy + INTIMA proliferation -> narrowing -> FURTHER INCREASE in PRESSURE
cor pulmonale
- RHF secondary to primary lung disease (lung disorder causes HTN)
physiological outcomes of pulmonary emboli (4)
- Circulatory collapse (BIG EMBOLI -> sudden cardiac death, heart cannot pump)
- Infarction (INTERMEDIATE emboli; RARE! -> only 10% of the cases bc bronchial artery supply still exists, lung is dual blood supply!)
- Pulmonary hypertension (RECURRENT, SMALL thromboemboli -> reduce pulmonary vasculature)
- V/Q mismatch (regardless of emboli size, as long as blood supply is cut off)
pathogenesis of pulmonary vasculitis
- inflammatory destruction of blood vessels
- cause bleeding into lungs -> HEMOPTYSIS
2 diseases with prominent lung manifestations
- Wegener granulomatosis -> affect nose, lungs, kidneys
- ChurgStrauss syndrome -> infiltration of many organs by EOSINOPHILS; pt usually has asthma
types of respiratory failure (3)
- Type 1
- Type 2
- COPD induced (pink puffers vs blue bloaters)
effects of respi failure (3)
- breathlessness (air hunger) -> due to hypoxia
- polycythemia (increase EPO production due to hypoxia)
- pulmonary arterial HTN (due to hypoxic vasoconstriction) -> secondary RH strain
what is type 1 respiratory failure & treatment
- hypoxaemia, NO hypercapnia (only some areas gas exchange affected, CO2 retention insignificant) -> alveolar capillary gas exchange affected, ventilation normal (eg pulm emolism/ pus in alveoli/ lung collapse/ fibrosis)
- can cause cyanosis
treatment
- give high pO2
what is type 2 respiratory failure
- hypoxaemia + hypercapnia
- poor ventilation -> cannot remove CO2
which 2 ways can type 1 respi failure lead to type 2 respi failure
- exhaustion or insufficient oxygen supply to the brain -> ventilation problems -> hypercapnia
- progression of disease (more of lung being affected) or exhausted -> compensatory measures (hyperventilation, tachycardia) fail -> hypercapnia
cause of pink puffers
- EMPHYSEMA
presentations
- hyperventilation due to less SA for gas exchange; use of accessory breathing muscles
- pink complexion
- barrel chest due to emphysema, flattened diaphragm on CXR
cause & presentation of blue bloaters
- CHRONIC BRONCHITIS
- hypoxemia + hypercapnia
- capillaries & alveoli undamaged but air CANNOT enter -> V/Q mismatch (no ventilation) -> deoxygenated blood
- R heart pumps harder to perfuse lungs better (but in vain) -> RH failure
Presentations
- cyanosis (deox blood around body) + overweight
- wheezing & crackles (bronchitis)
- elevated haemoglobin
what happens in chronic blue bloaters
- hypercapnia & hypoxemia tolerance increases -> dulls CO2 breathing reflex (FATAL)
what must be carefully given to blue bloaters
- oxygen -> dulling of CO2 driven breathing effect -> giving too much O2 can cause further decrease in ventilation rate -> O2 levels normal but CO2 builds up as breathing rate too slow to clear it -> acidosis
blue bloaters/ pink puffers treatment (4)
1) treat cause (eg infection)
2) give O2 (controlled in blue bloaters)
3) bronchodilators
4) assist ventilation (if necessary)
IMAGING: cardiac failure (4)
- cardiomegaly >0.55
- prominent interstitial markings (due to pulmonary edema) -> BAT WING appearance due to bilateral perihilar lung shadowing
- consolidations
- no costophrenic angle -> pleural effusion
IMAGING: causes of mass on Xray (3)
- granuloma
- primary lung carcinoma
- secondary metastases
IMAGING: posterior CXR vs anterior CXR
- PXR -> clavicle points sharply downwards
- CXR -> apex heart at 5th rib
IMAGING: supine vs upright CXR
- upright -> presence of gastric bubble
- supine -> no gastric bubble (CXR taken when person lying down, fluid fills entire gastric surface)
combination vaccines given in childhood to combat against 5 microbes (5)
Diphtheriae
Tetanus
Pertusis
Polio
Haemophilus influenzae
viral pathogens that can cause pneumonia (5)
- influenza
- adenoviruses
- rhinoviruses
- paramyxoviruses
- SARS/ coronavirus infections
lung diseases associated with asbestos (4)
Larynx
1. squamous cell carcinoma of larynx
Pleura
1. pleural plaque (benign areas of thickened tissue that form in the pleura or lung lining
2. malignant mesothelioma (pleural cancer)
Lung
1. progressive chronic lung fibrosis (abestosis) - parenchymal lung disease
