Lung Diseases😍

Localisation of Pathologies

  • Respiratory Epithelium Types
    • Location
      Epithelium Type
      Nasal mucosa till Proximal bronchiole
      Pseudostratified ciliated columnar epithelium
      Terminal bronchiole
      Ciliated cuboidal epithelium
      No goblet cells
      • Epithelium change
      No hyaline cartilage from here
      Respiratory bronchiole
      Non-ciliated cuboidal epithelium
      Alveolus
      Simple squamous epithelium
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  • Air bronchogram sign:
    • Differentiate between parenchymal and extra parenchymal pathologies.
    • Seen when:
      • The lungs are white.
      • The bronchi is patent (containing air - appears black).
    • Seen in intraparenchymal pathologies:
      • Consolidation.
      • Hyaline membrane disease.
      • Pulmonary edema
    • Absent in
      • Mediastinal mass
      • Pleural effusion

Consolidation vs Collapse

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Obstructive Lung Diseases (OLDs)

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COPD (Chronic Obstructive Pulmonary Disease)

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  • COPD primarily encompasses Emphysema and Chronic Bronchitis.
  • Both heavily associated with smoking.
  • Permanent damage to airways distal to the terminal bronchioles.
    • Damaged structures (collectively RDS):
      • Respiratory bronchiole
      • Alveolar duct
      • Alveolar sac

Microscopic Finding:

  • "floating septa" due to broken walls.
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Types:

Type of Emphysema
Affected Part
Lobe Involved
Common Association
Centriacinar
Central part
(respiratory bronchiole)
Upper lobe
Smokers

Most common clinically
Panacinar
All of RDS
(including alveoli)
Lower lobe
Alpha-1 antitrypsin deficiency
Distal Acinar
Distal part
(alveolar duct and sac)
Can cause spontaneous pneumothorax
Irregular
Irregular damage
(patchy involvement)
Most common histologically
(on autopsy)
GOLD Classification
GOLD Classification
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  • "pink puffers".
  • Physiology:
    • Inhalation is fine → exhalation of CO2 is problematic → air trappingenlarged lungs.

Radiological Finding: 

  • Flattening of the diaphragm.
    • notion image

Chronic Bronchitis

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  • Blue bloaters
  • Definition:
    • Productive cough
      • for at least 3 months in two consecutive years
      • with other causes ruled out.
  • Cyanosis (blue) → due to hypoxemia and hypercapnia.
  • Obesity + edema (bloater) → right heart failure (cor pulmonale).
  • Association:
    • Primarily smoking → increased mucus production.
  • Infections:
    • M/c H. influenzae in COPD patients.
  • Reid Index:
    • Ratio of submucosal glands / wall thickness.
    • In chronic bronchitis is > 40%
      • Normal Reid Index is < 0.4.
        • notion image

A/w cor pulmonale 

  • M/c chronic bronchitis > emphysema.
  • PAH + right-sided heart failure

CXR

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  • Hyperinflated lungs.
  • Flat diaphragm.
  • Tubular heart.
  • Barrel chest on lateral CXR.
  • DOC: Tiotropium
  • MOA: M3 Antagonist
  • Treats bronchoconstriction due to:
    • Parasympathetic overactivity (reversible component)
    • Fibrosis/sclerosis (irreversible component)
  • Side Effects
    • Dry mouth
    • Worsening of BPH

VLABA → COPD only

  • Olodaterol
  • Vilanterol
  • Carmoterol
  • Karma (Carmeterol) for Old (Olodaterol) Villains (Vilanterol)

New drugs COPD :

  • Roflumilast : PDE4 ⛔
  • Ensifentrine : Both PDE3 ⛔ and PDE4 ⛔
  • Rough (Roflumilast) Siphon (Ensifen)

Asthma

Genetics:

  • Gene for atopy: Chromosome 5q gene Polymorphism
  • At birth → TH2 Phenotype
    • Normally
      • switch to TH1 phenotype
      • due to exposure to many outdoor antigens
      • TH1 phenotype → Asthma disappears.
    • No exposure to allergens
      • Persistence of TH2 phenotype.
      • Persistence of TH2 phenotype → Asthma persists.
  • Associations: 
    • IL-13, ADAM33 gene polymorphisms.
      • Note: mutation of ADAMTS-13: TTP
  • Type 1 hypersensitivity (allergic) reaction.
  • IL-5 → Eosinophil mediated Pathology.

Features of Asthma:

  • Type I Respiratory Failure:
    • No CO2 retention seen.
    • No Type II respiratory failure.
  • No parenchymal involvement.
  • No diffusion defect.
    • Normal to ↑ DLCO.

Sputum Microscopy (The Three C's):

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  • Charcot-Leyden crystals:
    • Needle-shaped crystals made of galectin-10
    • derived from eosinophils.
    • Eda charley, needle vach easy aytt kalakku
  • Creola bodies:
    • Clusters of epithelial cells.
    • Sloughed mucus epithelium.
  • Curschmann spirals:
    • Whorled Mucus Plugs.
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Lung Finding:

  • Shows airway remodeling.

Micropathological Changes:

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  • Patchy Epithelial Necrosis
  • Sub-Mucosal Glandular Hyperplasia
  • Hypertrophy of bronchial smooth muscle
  • Reid's Index is normal.
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Classification
Symptom Frequency
Night Awakenings
Impact on Activity
FEV1 (% Pred.)
PEFR Variability
Recommended Treatment (GINA 2019)
Intermittent
< 2 episodes per month
None
Relievers (LABA) + 
ICS (if needed)
Mild Persistent
≥ 2 episodes per month
≥ 1 night/ month
Minor limitation
> 80%
< 30%
Relievers (LABA) +
Low dose ICS (Daily)
Moderate Persistent
Daily, not continuous
≥ 1 episode / week
Some limitation
60-80%
> 30%
Medium dose ICS (Daily) 
OR
Low dose ICS (Daily) 

LABA (Formetrol)
Severe Persistent
Continuous
Frequent
Significant limitation
< 60%
> 30%
High dose ICS (Daily) 

LABA (Formetrol)

GINA (GLOBAL INITIATIVE FOR ASTHMA) GUIDELINES

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Therapy Type
Drug of Choice (DOC)
Acute Attack (Rescue Therapy)
Inhalational formoterol +
Low dose inhaled corticosteroids
Maintenance Therapy
Formoterol + Low dose ICS
 

Brittle Asthma

  • Frequent, sudden, and life-threatening attacks
  • Occurs despite appropriate therapy

Types of Brittle Asthma

Type 1
Type 2
Persistent variability in PEFR
Normal or near-normal PEFR
Wide day-to-day fluctuations
Sudden unpredictable exacerbations
No obvious trigger
Management
Oral steroids
Infusion of bronchodilators
Dietary exclusion of allergens
Management
• Respond only to
subcutaneous epinephrine
Extrinsic Asthma
Intrinsic Asthma
• Atopic → childhood onset
• Boys > Girls
Adult Onset
Type I Hypersensitivity
Negative Skin Test
↑ IgE levels Eosinophils
Normal IgE levels
Associated with:
Allergic Rhinitis
Atopic Dermatitis
Super antigen: 
Staph Aureus Enterotoxin
MC allergen :
Dermatophagoides (House dust mites)

Samter's Triad :
Adult onset Asthma
Aspirin Intake
Nasal Polyps
Bad Prognosis
Males = Females
  • Airway Hyperresponsiveness assessed by
    • MCT (Methacholine Challenge Test).
  • IgE levels
    • RAST (Radio AllergoSorbent Test).
  • Non Invasive Test to assess airway inflammation
    • Fractional Exhalation of Nitric Oxide (FeNO).

Pulmonary Function Tests:

  • ↓ FEV1/FVC ratio.
Response
Response to inhaled β2 agonist
12% in FEV1, 
200mL
β2 → 12
Diurnal variation in PEFR/FEV
> 20%.
24 hrs → 20
Exercise challenge
> 15% in FEV1.
Acute Severe Asthma
Life-threatening Asthma
Dyspneic, Speaks in words
Altered mental status with drowsiness.
Agitated Patient
Exhaustion, Cyanosis
Loud wheeze throughout Respiration
Silent Chest (Absent chest sounds)
Mute
Respiratory Rate = 30/min
RR > 30bpm (in adults)
RR > 60bpm (in children)
Peak Expiratory Flow 25-40 ml/min
PEFR < 25% predicted or best.
Accessory muscles are used
Poor respiratory effort.
Heart rate > 120 : Tachycardia
Hypotension, Arrhythmia,
Relative Bradycardia
Pulsus Paradoxus (+)
Sp02 < 90%.
PaO2 < 8 kPa; < 60mmHg of Hg
PaCO2: < 40 mmHg.
Paradoxial
PaCO2 is normal (4.6-6 kPa)
Paradoxical Breathing
Relative Bradycardia
No pulsus paradoxus

Peak expiratory flow meters

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  • Portable, hand-held devices
  • Used at home for monitoring PEFR
  • Increase diurnal variability of PEFR (peak expiratory flow rate) >13%

Treatment of asthma in children

  • As per the latest GINA (Global Initiative for asthma),
    • All children with Bronchial Asthma
      • daily dose ICS + SABA
      • either Symptom driven or daily.
    • No role of SABA only Rx in managing acute exacerbations
      • It increases r/o exacerbations

Metered dose inhaler

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  • Used in drug delivery in children with bronchial asthma
  • Parts
    • Blue colored structure:
      • Metered dose inhaler,
      • Contains bronchodilator
    • White-colored structure:
      • Spacer,
      • Must since it improves in drug delivery
    • Baby mask:
      • Required in < 4 years age children.

Management of status asthmaticus in a child

  • Medical emergency
  • Also known as acute severe asthma
  • The pulmonary index score is used for the assessment of the severity
  • Primary management
    • airway, breathing and circulation
    • (Chest x-ray and ABG to look for ventilation therapy)
  • Start oxygen therapy and admission
  • Continuous nebulization
    • levosalbutamol/MDI
  • Start systemic steroids
    • Inj. hydrocortisone f/b oral prednisolone
    • Ipratropium nebulization can be used
  • In case of no improvement:
    • Inj. Magnesium sulfate,
    • theophylline
    • ketamine

Bronchiectasis

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  • Definition: Dilation of the bronchi and bronchioles.
  • Causes:
    • Genetic: Most famously, Kartagener Syndrome.
    • Acquired: Obstruction (e.g., foreign body) or bacterial infection (e.g., sepsis).
  • Kartagener Syndrome:
    • Defect: Dynein defect of cilia.
    • Dynamic (Dynein defect) Kart (Kartagener)
    • Triad:
        1. Bronchiectasis
        1. Sinusitis
        1. Situs inversus (e.g., dextrocardia)
    • Important Additional Finding: Associated with male and female infertility.
  • Location:
    • M/c in Left Lower Lobe
    • LL > UL
  • Investigation: 
    • HRCT  is the definitive investigation.
  • Radiological Finding: Classic "tram track appearance".
    • Note: A "tram track appearance" can also be seen on microscopic examination in MPG type 1 (a renal disorder).
    • MP (MPGN) runs in a Kart (Kartagener) through Tram track ()
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  • Dilatation of bronchi.
  • Normally, bronchus tapers down peripherally.
  • In Bronchiectasis
    • no tapering → bronchi remain parallel
    • Tram track sign
      • notion image
    • Signet ring sign:
      • Vessel adjacent to the dilated bronchi.

Kartagener Syndrome

  • Bronchiectasis associated with situs inversus
    • Kartagener's syndrome
      • notion image

Interstitial Lung Disease

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  • Military (Miliary) people
    • get TB
    • Laugh (Loeffler’s)
    • Heal by eating chicken (healed varicella)
    • make History (Histoplasmosis)
  • Presentation:
    • Usually a female patient
    • dry cough, shortness of breath
    • associated with connective tissue disorder.
  • M/c type
    • Idiopathic pulmonary fibrosis
UIP/IPF pattern
UIP/IPF pattern
  • IOC - HRCT.
    • UIP/IPF pattern
      • Honeycombing pattern +
      • Basal Lower lobe dominance +
      • Traction bronchiectasis
    • Ni thanna (Nintendanib) Feni done (Pirfenidone) ayi → lung fibrosis ayi (IPF)
      • Perfenidone
Nintendanib
        Perfenidone
        Nintendanib
      • TGF α → KGF α → Menetriers disease
      • TGB β → KGF β → drink Feni
      • Ninte Dani → PD Girl Friend (PDGF)

Crazy pavement appearance:

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  • Interlobular septal thickening is seen with ground glass opacity.
  • no air filled cavities are seen.
  • Seen in Pulmonary alveolar proteinosis >>> COVID 19
  • Mnemonic: Crazy Pappu (PAP) in pavement

Cystic Bronchiectasis

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  • Some of these dilated bronchi contain mucus.
  • Bronchi appears as cysts.
  • Bunch of grape appearance.

Pulmonary Alveolar Proteinosis

  • Interstitial lung disease
  • Due to defective pulmonary macrophage function
  • Leads to accumulation of surfactant in alveoli and bronchioles
  • Autoantibodies against GM-CSFmost common cause
  • Clinical features
    • Progressive dyspnea
    • Cough with chunky, gelatinous sputum
      • PAS-positive
  • Histology
    • Alveoli filled with:
      • Pink, Dense, Homogeneous, Amorphous material
    • Alveolar walls intact
    • Surfactant proteins:
      • Demonstrated by IHC
  • HRCT: Crazy pavement appearance

Pneumoconiosis

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  • Pneumoconioses are occupation-related lung diseases.
  • Mostly involve upper lobe of lung.
    • Exception
      • Asbestosis → affect lower lobe
  • Restrictive lung diseases.
  • All notifiable except bagassosis.

Range of Dust Particles

Size (micron)
Effect
5-10
Lodged in upper respiratory tract
3-5
Lodged in lower respiratory tract
Cause pneumoconiosis
1-3
Lodged in alveoli
Cause pneumoconiosis
<1
Diffusible
  • Note: 1-5 micron sizes cause pneumoconiosis

Types

Disease
Particle
Source
Silicosis
Silica
Sand stone, granite, pottery and ceramic industry,
gold, mica and steel industry.
Asbestosis
Asbestos
Asbestos cement factory, fireproof textiles.
Anthracosis
(Black lung)
Coal dust
Coal mines.
Byssinosis
Cotton dust
Textile industries.
Cotton business
Bagassosis
Sugar cane dust
(Bagasse)
• Inhalation of Thermoactinomyces sacchari
Bag of sugar

Silicosis vs Asbestosis

Silicosis
Asbestosis
Cause
Silica dust
Asbestos fiber
Affects
upper lung zone
Lower lung zone
Leads to
Alveolitis
Bronchiolitis
X-ray
Snow storm appearance
Ground glass appearance
Association
TB complication
Bronchial CaM/C

Mesothelioma Most specific
silica - snowstorm
AsBastosis - Base, Ground Bronchilolitis,

Harmful Chemicals

Chemicals
Disease
Benzene, Ethylene Oxide
Leukemia
Benzidine
Bladder cancer
Beryllium, Cadmium, Chromium, Radon, Silica, ionizing radiation, Nickel
Lung cancer
Arsenic
Skin, lung, liver cancer
PAH
(Polycyclic Aromatic Hydrocarbon)
Skin, scrotum and lung cancer

Aromatic - skin , scrotum, lungs
Vinyl chloride
(
PVC plastic)
Liver cancer
Wood dust, Nickel, Chromium
Nasal sinus problems

Different color() nikker() itt wood() panikk poi sinusitis vann
 

Silicosis

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  • Most common pneumoconiosis.
  • glass industry, sandblasting industry
    • Progressive massive nodular fibrosis → Upper lobe
  • Lymph Node:
    • eggshell calcification in the lymph nodes.
  • increased risk of TB and lung cancer.
  • Silly (Silicosis) people are like egg shell () and glass ()
  • Egg (Egg shell) beaten on a glass (glass industry) → bubble (nodular fibrosis) when heat
  • Egg shell calcification:
    • Peripheral Calcification around lymph nodes
      • hilar lymphadenopathy
      • also in silicosis., Sarcoidosis, Post radiation therapy lymph nodes

COALWORKERS PNEUMONIA

  • Industry Association: Related to the coal industry.

Progression (Three Steps):

1. Anthracosis:

  1. Just black lungs with no symptoms.
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  • Definition: Inhaled carbon.
  • Appearance: Black color lungs.

2. Simple CWP:

  • Development of centriacinar emphysema.
  • Mnemonic: Coal smoke has 'S' sound, like smokers, hence centriacinar

3. Complicated CWP:

  • Results in fibrosis.
  • Kaplan Syndrome
    • CWP + rheumatoid arthritis.
  • Note: Felty syndrome
    • notion image
  • X ray
    • Upper lobes opacities
  • We Felt (Felty syndrome) pain fo RA () ENT pg → We gave him a cap (Caplan)
  • NOTE:
    • Erasmus syndrome: CWP + Systemic sclerosis
    • Erase & Cap → CWP syndromes
    • EraSS → Systemic sclerosis

ASBESTOSIS

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Frozen Hemithorax → No mediastinal shift → Hallmark of mesothelioma
Frozen HemithoraxNo mediastinal shift → Hallmark of mesothelioma
  • Location:
    • Affects the lower lobe of the lung.
      • Mnemonic: "Basetosis" for base/lower lobe
  • Forms:
    • Amphibole / CrocidoliteGood Prognosis
      • Mnemonic: Amphibian, like a crocodile, lives in land and water
    • Serpentine / Chrysotile.
      • Snake → Cry
  • High-resolution computed tomography (HRCT)
    • "honeycombing"
  • Associated Cancers:
    • Most common cancer: 
      • Adenocarcinoma lung.
    • Most specific cancer: 
      • Mesothelioma → Frozen Hemithorax (Hallmark)
      • notion image
  • Associated with
    • Shipyard industry
    • Cement industry
  • Mnemonic: Basetosis → Mesayude (Mesothelioma) adiyil (adenocarcinoma) Dumbell (asbetos bodies), made of iron (ferruginous bodies) → long vili vilichu (branched long filaments on E/M)
  • Microscopic Finding:
    • Characterized by pleural plaque and pleural nodules containing dumbbell-shaped asbestos bodies (ferruginous bodies).
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  • Occupational lung disease - M/c shipyard industry.
  • Mnemonic: Asbestos → Holly leaf → comet tail
  • M/c radiological finding:
    • Calcified pleural plaques - Holly leaf sign.
      • Base of lung/Diaphragmatic pleura is affected.
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  • On CT:
    • Comet tail sign:
      • Rounded opacity
      • vessels pulled towards it
      • seen in round atelectasis.
    • The white opacity seen along the pleura are the plaques.
      • notion image
  • Can give rise to Mesothelioma.

Note: Other structures with dumbbell shapes in pathology/radiology:

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  • Calcium oxalate monohydrate crystals (renal pathology).
  • Spinal schwannoma (radiology).
  • Pox virus DNA (microbiology).


  • Byssinosis:
    • Exposure to cotton or organic dust.
    • Mnemonic: Business → cotton
  • Bagassosis:
    • Exposure to sugarcane dust.
    • Mnemonic: Bagil sugar
  • Berylliosis:
    • Exposure to beryllium.
    • Microscopic Finding: Shows non-caseating granulomas, Monocytic
    • Jewellery /dental alloy
    • Granulomatosis → Similar to sarcoidosis
    • BeLPT → Beryllium Lymphoproliferative test
    • HLA-DP
  • Cobalt exposure
    • Diamond industry
    • Giant cell interstitial pneumonitis
    • cobelt - belt ilu diamond it is giant
  • Stannosis:
    • Exposure to tin.
  • Siderosis:
    • Exposure to iron.

Extrinsic Allergic Alveolitis / Hypersensitivity Pneumonitis

Definition

  • Repeated inhalation of organic antigens in dusts.

Pathogenesis :

  • Both Type 3 and Type 4 hypersensitivity.

Causes & Examples

Lung Condition
Antigen
Bird fanciers' lung
Avian proteins
Farmer's lung
Saccharopolyspora rectivirgula spores
Malt workers' lung
Aspergillus clavatus
Mushroom workers' lung
Thermophilic actinomycetes

Investigations

  • Chest X-ray: 
    • Diffuse micronodular interstitial shadowing.
  • CT
    • Ground glass appearance
      • notion image
  • Broncho-alveolar lavage: 
    • Lymphocytosis.
  • Blood: NO eosinophilia.

Differences between HP & Allergic Bronchopulmonary Aspergillosis (ABPA)

Feature
Allergic Bronchopulmonary Aspergillosis (ABPA)
Hypersensitivity Pneumonitis (HP)
Pathology
Colonisation of airway

Eosinophilic inflammation

- Hypersensitivity (I + III)
Non caseating granulomas

Lymphocytic inflammation

Hypersensitivity (IV > III)
Radiographic Features
Bronchiectatic changes

Migratory infiltrates
Diffuse infiltrates →  Reticulonodular opacities

Bilateral GGD & nodular opacity

CT: Mosaic tiles attenuation
Skin test reaction to aspergillus antigens
+ve (A. fumigatus)
+ve (A. clavatus)
Peripheral eosinophilia
+ve
-ve
IgG Aspergillus precipitins (Type III hypersensitivity)
+ve
+ve
Serum IgE levels
↑↑ (Significantly increased)
Normal

Aspergillus lungs:

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  • A fungus with septate and acute angle branching hyphae.
  • Can cause:
    • Allergic Bronchopulmonary aspergillosis (ABPA).
    • Aspergilloma.
    • Angio invasive aspergillosis.

ABPA:

  • Dilated central bronchi filled with mucous - Finger in glove sign.
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Aspergilloma:

  • Seen when there is a pre existing cavity in the lung.
  • Air crescent sign or monod sign.
  • Prone CT to confirm aspergilloma:
    • fungal ball is mobile
    • comes to the dependent position.
      • notion image

Angio Invasive Aspergillosis:

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  • Central infarct surrounded by GGO - Halo sign.
  • i.e. white consolidation surrounded by ground glass opacity.
  • Seen in immunocompromised patients.
  • Voriconazole

Mucormycosis lungs

  • Also called: Black fungus
  • Reverse HALO sign (Atoll sign) → centre dark, periphery light
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  • Reverse halo sign on CT
  • Neutropenia
  • Immunocompromised
  • Hyphae: Aseptate, Right angle, Broad, ribbon-like
  • Culture:
    • Lid-Lifters (SDA)
    • May be negative d/t Hyphal fragility (killed by tissue homogenisation)
  • Lid lift cheyyumbo mukki povum
  • Treatment
    • Surgical resection
    • Amphotericin B +/- Posaconazole
    • Mucus pasha pole - Posaconazole
  • Negative Staining Group:
    • Blastomyces, Mucorales, Cryptococcus
    • Banglore Medical College
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ARDS

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Patchy consolidation ⇒ ARDS
Pulm edema → 1st sign → cephalisation
Patchy consolidation ⇒ ARDS
Pulm edema1st signcephalisation

Criteria

  • ARDS is known by various names:
    • Acute Lung Injury
    • DAD
    • Blast Lung
    • Acute Alveolar Injury

Berlin Definition 2012

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  • Acute onset: 
    • Within 1 week of clinical insult/worsening respiratory symptoms.
  • Chest X-ray: 
    • Bilateral alveolar/interstitial infiltrates not explained by effusion/collapse/nodules.
  • Non-cardiogenic: 
    • Normal ECHO.
  • Oxygenation:
    • Severity
      PaO₂/FiO₂
      Mild
      200 - 300
      Moderate
      100 - 200
      Severe
      < 100

Factors Preventing Pulmonary Edema

  • Retained intravascular protein.
  • Interstitial lymphatics drain fluid.
  • Tight junctions between epithelial cells.

Etiology

  • Primary ARDS:
    • Pulmonary sepsis.
    • Massive blood transfusion.
    • Acute pancreatitis.
    • Transfusion-Associated Lung Injury (TRALI).
    • Smoke inhalation.
    • Drowning.
    • Post-surgery.
  • Secondary ARDS:
    • Non-pulmonary sepsis (UTI, surgical site infection).
    • Major trauma/burns.

Pathogenesis

  • Toxin/sepsis → Alveolar epithelial injury → Release IL 1, IL 6, TNF α → Neutrophil recruitment and Damage of Capillary endothelium → Protein + Fluid coming out of endothelium → Air spaces filled with bloody proteinaceous fluid with loss of Surfactant → Pulmonary Edema → Hypoxia

Pathological Phases

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  • 1. Acute Exudative Phase (1st week):
    • Diffuse alveolar damage (DAD):
      • Interstitial + alveolar edema.
    • Eosinophilic hyaline membrane deposition is the hallmark.
    • Also known as hyaline membrane disease.
  • 2. Fibroproliferative Phase (2nd week).
  • 3. Fibrotic Vasoconstriction (3rd week).

Clinical Features

  • Rapid onset dyspnea.
  • Hypoxemia.
  • Bilateral crackles: Diffuse pulmonary infiltrates.
  • Tachypnea, tachycardia, diaphoresis.
  • Pulmonary hypertension: Due to hypoxemic vasoconstriction.

Mechanical Ventilation

  • Mainstay of treatment.
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  • Inverse ratio ventilation with inspiration.
  • Prone ventilation.
  • Permissive hypercapnia.

VILI (Ventilation-Induced Lung Injury)

Pathogenesis
Treatment
Volume trauma:
• ↑ Lung volume → Alveolar injury
Low tidal volume ventilation.
(High frequency ventilation)
Barotrauma:
• ↑ Transpulmonary pressure
Low plateau pressure.
(Low driving pressure)
Atelectotrauma:
Collapse and de-collapse during tidal breathing
High PEEP

Respiratory Failure

Type
Key points
Type I
Acute hypoxemic respiratory failure
• Low pO2
• Normal / low pCO2
Type II
Hypoxemia with hypercapnia
• Low pO2
• High pCO2
Type III
Peri-operative respiratory failure
• Seen after general anesthesia
Due to decreased functional residual capacity
Type IV
Shock-related respiratory failure
Hypoperfusion of respiratory muscles
• Seen in
cardiogenic shock

Pleural Effusion

(Light, REM and PEM)

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  • IOC - USG.
  • Best X-ray view: Ipsilateral decubitus view.
  • Light’s criteria for exudative effusion:
      1. Pleural fluid protein/serum protein >0.5
      1. Pleural fluid LDH/serum LDH >0.6
      1. Pleural fluid LDH >2/3rd upper reference limit of normal for serum.

Low glucose

  • low glucose in RUM (REM)
    • RA
    • Empyema
    • Malignancy

High Amylase

  • Pancreatitis
  • Esophageal rupture
  • Malignancy
 

Pleural effusion vs Hydropneumothorax

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  • Pleural effusion:
    • Ellis's curve.
    • Blunting of costophrenic angle.
  • Hydropneumothorax:
    • Horizontal air fluid level.
  • Lateral decubitus X-ray
    • Done for pleural effusion.
      • Fluid comes to the dependant side.
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  • Pleural effusion signs:
    • Most sensitive
      • USG (5 - 10 mL) >
      • I/L lateral decubitus > Lateral > CXR PA erect > Supine (500 ml)
    • On chest X-ray:
      • Ellis's curve.
      • Blunting of costophrenic angle.
        • due to accumulation of fluid.
    • On CT scan (in supine):
      • Fluid gravitates posteriorly.
        • Appears gray in color.
          • notion image
    • Most sensitive investigation:
      • USG.

Infected pleural effusion (empyema)

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  • Empyema causes thickening of surrounding pleura:
    • Split pleura sign.
    • notion image
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Chylothorax

Chylothorax

  • L subclavian vein catheterization
  • Lymphatic leaks
  • Triglyceride > 110 mg/dl
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Pseudo chylothorax

  • Seen in RA
  • Normal TGCholesterol crystals +

Pulmonary Thromboembolism (PTE)

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Causes of Thrombosis

  • Inherited:
    • Factor V Leiden mutation – most common.
  • Acquired:
    • Antiphospholipid antibody syndrome – most common.
    • Nephrotic syndrome.
    • Post-orthopedic surgery.
    • Malignancy – adenocarcinoma.
    • COPD.
    • Pregnancy – pelvic veins.

Sites of Thrombosis

  • Deep veins – most common femoral vein (supra-popliteal).
  • Calf veins.
  • Pelvic veins – in pregnancy.

Types of Pulmonary Embolism

  • Massive Hypotension present.
  • Submassive – No hypotension, ± RV dilatation.
  • Non-massiveNo hypotension, no RV dilatation.

Symptoms

  • Most common – Unexplained dyspnea.
  • Syncope.
  • Pleuritic chest pain.
  • Cough with hemoptysis.
  • Sudden cardiac death.

Risk Assessment

  • Well’s score – assesses likelihood.
    • Score > 4 → CTPA
    • Score < 4 → D dimer
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Diagnosis

  • CT Pulmonary Angiography (CTPA) – gold standard.
  • D-dimer – for low-risk patients.
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Pulmonary Embolism Radio

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McConnel Sign
• RV free wall → Hypokinetic
• RV Apex → Hyperkinetic
McConnel Sign
• RV free wall → Hypokinetic
• RV
Apex Hyperkinetic
  • Predisposing factor: DVT — Bedridden patients/immobilized patients.
  • Screening investigation: D-dimer (raised).
  • IOC - CTPA/CECT.
    • Contrast filling defect is seen.
  • X-ray Signs
    • Palla sign: Enlarged right descending pulmonary artery
      • notion image
    • Hampton's hump: Infarct formation.
    • Westermark sign: Focal oligemia.
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Pneumonia

MCC
Organism
Typical CAP
S. Pneumonia
Atypical CAP
Mycoplasma
HAP (> 48hrs of admission)
Gram -ve
VAP (> 48hrs of ventilation)
• Early: S. Pneumonia
• Late:
Pseudomonas
• Nowadays:
Acinetobacter

CURB-65 Scoring

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WHO IMNCI PROTOCOL

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  • Cough/cold:
    • No pneumonia.
    • Home care advice.
  • Fast breathing/chest indrawing:
    • Pneumonia.
    • Oral amoxicillin/home care advice.
    • Reassessed after 48 hours.
      • If the child has worsened, refer to a higher center.
  • General danger signs:
    • Severe pneumonia/very severe disease.
    • First dose antibiotic/referral for injectable antibiotic
      • 1st dose of Inj. Ampicillin and Gentamycin

SAANS PROTOCOL:

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  • Social Awareness & Action to Neutralize Pneumonia Successfully.
  • Launched in 2019 to reduce deaths due to childhood pneumonia.
  • For 2-59 months child with cough +/- difficult breathing.

Management

Condition
Signs → SAANS Protocol
Severe pneumonia/
very severe disease
General danger signs
Convulsions
Lethargy
Inability to drink or breastfeed
Persistent vomiting
Unconsciousness
Stridor in a calm child

OR

Chest indrawing
Pneumonia
Fast breathing:
- < 2 months: ≥ 60 breath/min
- 2–11 months: ≥ 50 breaths/min
-
12–59 months: ≥ 40 breaths/min
No pneumonia/cough or cold
No signs of severe pneumonia or pneumonia

Severe Pneumonia

  • ASHA:
    • Pre referral dose of Oral amoxicillin + referral.
  • CHO (Community Health Officer):
    • Oral amoxicillin + IM Gentamicin + Hospitalization/Referral
Important
If SAANS protocol is mentioned → Refer
If not mentioned → WHO → Oral amox for 5 days
Important
If SAANS protocol is mentioned → Refer
If not mentioned → WHO → Oral amox for 5 days

Klebsiella Pneumonia:

  • Bulging fissure sign:
    • Horizontal fissure is curved.
      • notion image

Pneumatocele:

  • Cavity filled with air.
    • Staphylococci
    • PCP (HIV +)
      • Pneumatocele + ground glass opacityperihilar region.
        • notion image

Congenital pulmonary malformations

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