Lecture 2 Flashcards

(41 cards)

1
Q

What is agenisis, Aplasia and hyperplasia

A

Agenisis: complete absence of a lung or lobe with absent bronchi
Aplasia: absence of lung tissue but presence of rudimentary bronchus
Hypoplasia: presence of both bronchi and alveoli in an underdeveloped lobe

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2
Q

What are obstructive lung diseases

A

OLD: obstruction of air flow, air trapping in lungs, due to premature airway closure includes COPD, asthma and bronchiectasis.

Chronic obstructive pulmonary disease: often due to tobacco use or allergens often associated with viral or bacterial upper respiratory tract infection.

Chronic bronchitis: productive cough for more than 3 months. We have hypertrophy and hyperplasia of mucus secreting glands in bronchi

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3
Q

What are some disorders associated with airflow obstruction

A
  • chronic bronchitis ( mucous gland hyperplasia)
  • bronchiectasis ( airway dilation or scarring)
  • asthma ( smooth muscle hyperplasia excess mucous, inflammation
  • emphysema ( air space enlargement, wall destruction)
  • small airways disease ( inflammatory scarring)
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4
Q

What is emphysema and DLCO

A

Alveolar wall destruction -> damage to alveolar capillary membrane
Centriacinar - associated with tobacco smoking and seen in upper lobes
Panacinar - effects lower lobes and associated with alpha 1 antitrypsin deficiency

DLCO: lung diffusion test, used asses lungs ability to transfer gas from inspired air to blood stream

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5
Q

What are the types of emphysema

A

1) centracinar
2) panacinar
3) paraseptal
4) mixed and unclassified

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6
Q

Symptoms of emphysema

A

Coughing without phlegm
Fatigue
Wheezing
Barrel like chest
Difficulty sleeping

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7
Q

Chronic bronchitis

A

Chronic airway inflammation
Bronchial tubes in lungs inflamed causing productive cough
If we have exposure to irritants then it can cause the hypertrophy of bronchial mucous glands causing more mucous production

Risk factors are: smoking, cystic fibrosis and genetics

Complication: pulmonary hypertension, right ventricle increased load

Symptoms: wheezing and hypoxemia

Diagnosis: chest X ray, ABGs

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8
Q

What is asthma

A

Coughing, tight chest, difficulty breathing.

It is triggered by allergens, associated with atopy, type 1 hypersensitivity, smooth muscle hypertrophy and hyperplasia

ACUTE: Allergen -> production of CD4 and Th2 then we have the release of IL4 and IL5 then esinophils and mass cells release inflammatory mediators

CHRONIC: scarring, fibrosis causing thickness of the epithelial basement membrane, permanent narrowing causing Th2 cells to release IL5.

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9
Q

COPD VS ASTHMA

A

COPD: not fully reversible, mostly causing be smoking, symptoms are often constant and progressive, productive cough higher neutrophil level

ASTHMA: fully reversible, not really caused by smoking , symptoms are recurrent episodes, dry cough, higher esinophil level

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10
Q

Asthma and COPD

A

COPD: not fully reversible, mostly causing be smoking, symptoms are often constant and progressive, productive cough higher neutrophil level

ASTHMA: fully reversible, not really caused by smoking , symptoms are recurrent episodes, dry cough, higher esinophil level

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11
Q

What is bronchiectasis

A

Pulmonary infection combined with obstruction or impaired clearance causing permanently dilated airways: Chronic cough,
Caused by airway obstruction, cystic fibrosis,

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12
Q

What are some characteristics of Kartageners syndrome

A
  • bronchiectasis
  • chronic sinusitis
  • situs inversus totalis

This is the triad

Infertility is a diagnosis

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13
Q

What is idiopathic pulmonary fibrosis

A

Abnormal pulmonary healing process causing excess deposits of collagen -> progressive scarring of lung tissue-> lung function declines
Also we could have over proliferated type 2 pneumonocytes -> excess collagen and it accumulates-> restriction of lung expansion

Digital clubbing, crackles

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14
Q

What is sarcoidosis

A

Widespread of non caseating granulomas, elevatedACE and CD4 and CD8
Associated with bell palsy

SCHAUMANN & ASTEROID bodies, RHEUMATOID arthritis, high CALCIUM, OCULAR uveitis, INTERSTITIAL fibrosis, vitamin D activation, SKIN changes

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15
Q

How do we diagnose sarcoidosis

A

Ct scan
Non caseating granulommas disorder
Panda sign: in Ga scan, in bilateral and paratoid gland

Lambda sign: increased uptake of radionuclide right paratracheal lymph nodes

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16
Q

What is hypersensitivity pneumonitis

A

Mixed type III/ IV HS reaction to environmental triggers like actinomyces and aspergillus, seen in farmers, chronically leads to irreversible fibrosis

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17
Q

What is pneumoconiosis

A

ASBESTOS RELATED DISEASE: like pulmonary fibrosis associated w pleural plaques, increased risk of caplan syndrome, effects the lower lobes

BERYLILOSIS: associated w exposure to beryllium we see granulomas so it it responsive to glucocorticoids, affects upper lobes

COAL WORKERS: prolonged coal dust exposure, increased risk of caplan syndrome, affects upper lobes. Anthracosis ( asymptotic, found when there is exposure to sooty air)

SILICOSIS: associated w sandblasting and foundries mines macrophages respond to silica and release fibrogenic factors leading to fibrosis. We can see eggshell calcification on lymph nodes

18
Q

What is pneumonia

A

Infection of one of both of the lungs, characterised by inflammation of alveoli

19
Q

Types of pneumonia

A

Lobular: S pneumoniae, legionella and Klebsiella and it make involve the entire lobe or the whole lung

Bronchopneumonia: S pneumoniae, S aureus, H influenza, klebsiella- acute inflammatory infiltrates from bronchus into alveoli

Interstitial: mycoplasma, chlamydia etc. diffuse patchy inflammation to interstitial areas at alveolar walls

Cryptogenic organising: does not respond to antibiotic but responds to glucocorticoids- noninfectious, inflammation of bronchioles

Aspiration: aspiration of oropharyngeal or gastric contents it can progress to abscess

Aspiration (chemical) - hours after aspiration event due to gastric acid inflammation

20
Q

What is the natural history of lobular pneumonia

A

Day 1-2: congestion ( red purple parenchyma)
Day 3-4: red hepatization ( red brown consolidation, exudate with fibrin, bacteria, RBCs and WBCs
Day 5-7: gray hepatizaton, exudate filled with WBCs RBCs and fibrin
Day 8+: resolution, enzymatic digestion of exudate by macrophages

21
Q

What is community acquired pneumonia

A

Acquired outside hospital setting caused by S pneumoniae, S areus, H influenza etc
Risk: advanced age, low immunity, smoking, malnutrition

High fever, cough, dullness on percussion

22
Q

What is pulmonary hypertension and the etiologies

A

Definition: Elevated mean pulmonary artery pressure > 20 mm Hg at rest.
• Results in:
• Arteriosclerosis
• Medial hypertrophy
• Intimal fibrosis
• Plexiform lesions
• ↑ Pulmonary vascular resistance → ↑ RV pressure → RVH → RV failure

Etiologies (Groups 1–5):
1. Group 1: Pulmonary Arterial Hypertension (PAH)
• Often idiopathic; more common in females.
• May involve BMPR2 gene mutation → abnormal smooth muscle proliferation.
• Endothelial dysfunction → ↑ vasoconstrictors (e.g., endothelin), ↓ vasodilators (NO, prostacyclins).
• Causes: drugs (e.g., cocaine), connective tissue disease, HIV, portal HTN, congenital heart disease, schistosomiasis.
2. Group 2: Left Heart Disease
• Due to systolic/diastolic dysfunction or valvular disease.
3. Group 3: Lung Diseases or Hypoxia
• From lung parenchymal destruction (e.g., COPD), fibrosis, hypoxic vasoconstriction (e.g., OSA, high altitude).
4. Group 4: Chronic Thromboembolic
• Recurrent microthrombi → ↓ cross-sectional area of pulmonary vascular bed.
5. Group 5: Multifactorial
• Due to hematologic, systemic, or metabolic disorders, or tumor compression.

23
Q

What is lung abscess

A

Localised collection of puss within parenchyma, caused by aspiration of oropharyngeal contents

24
Q

What is acute respiratory distress syndrome

A

Alveolar insult (e.g. infection, trauma, etc.) triggers the immune system.
2. This causes release of pro-inflammatory cytokines, which attract and activate neutrophils.
3. Neutrophils release toxic substances (like reactive oxygen species and proteases).
4. These substances damage the capillary endothelium, increasing blood vessel permeability.
5. Protein-rich fluid leaks into the alveoli, leading to:
• Hyaline membrane formation (from fluid and dead cells)
• Noncardiogenic pulmonary edema (fluid buildup not due to heart failure; PCWP is normal)
6. This results in:
• ↓ Lung compliance (lungs become stiff)
• Ventilation-perfusion (V/Q) mismatch (oxygen can’t pass into the blood properly)
7. Hypoxic vasoconstriction occurs (body tries to redirect blood to better-ventilated areas), which increases pulmonary vascular resistance.
8. Loss of surfactant (a substance that keeps alveoli open) worsens alveolar collapse, especially in:
• Preterm infants
• Drowning victims

Cause is sepsis, consequences is low like compliance and pulmonary hypertension

25
What is pneumothorax and different types
Definition: • Air in the pleural space → lung collapse • Symptoms: • Dyspnea (shortness of breath) • Uneven chest expansion • Chest pain • ↓ Tactile fremitus, hyperresonance, ↓ breath sounds on the affected side ⸻ Types of Pneumothorax: 1. Primary Spontaneous Pneumothorax • Cause: Rupture of apical blebs/cysts • Most common in: Tall, thin, young males • Linked to smoking 2. Secondary Spontaneous Pneumothorax • Cause: Underlying lung disease (e.g., emphysema, Marfan syndrome, infections) • Can also result from barotrauma in mechanical ventilation 3. Traumatic Pneumothorax • Cause: Blunt or penetrating trauma (e.g., rib fracture, gunshot, iatrogenic like central line or lung biopsy) 4. Tension Pneumothorax (Life-threatening) • Air enters but cannot exit the pleural space • Leads to rising intrathoracic pressure → • Tracheal deviation (away from affected side) • Mediastinal shift • ↓ Venous return → ↓ cardiac output • Obstructive shock: hypotension, tachycardia, JVD • Emergency: Needs immediate needle decompression + chest tube placement
26
What is pleural effusion
Excess fluid accumulated in pleural space so we have restricted lung expansion. Transudative pleural effusion: pressure driven infiltration, increased hydrostatic pressure. Clear fluid due to increased hydrostatic pressure Educative pleural effusion: local inflammatory processes-> leaky capillaries. Cloudy fluid due to infection
27
What is atelectasis
Alveolar collapse Causes: - obstruction of airway stops new air from reaching distal airways - compressive: external compression on lung decreases lung volume - contraction: scaring of lung parenchyma - adhesive: lack of lung sufactant
28
What is a pulmonary embolism
Definition: Blockage of pulmonary arteries by: • Thrombus (blood clot) • Fat embolus • Air embolus • Tumor tissue • Embolus: A clot or plug that travels through the bloodstream and blocks a smaller vessel, disrupting blood flow • Emboli travel to the lungs and lodge in pulmonary vessels • Size and number of emboli determine where they get stuck • This causes obstruction of blood flow → ↓ perfusion to part of the lung • That lung area is still ventilated (air enters), but not perfused (no blood flow) • → This leads to a ventilation-perfusion (V/Q) mismatch • → Hypoxemia (low oxygen in the blood) results
29
Risk factors of pulmonary embolism
Most PE cases come from thrombi (clots) that form in: • Deep veins of the calf, femoral, popliteal, or iliac regions (DVT) • Other emboli sources include: • Tumors, fat, air, bone marrow, amniotic fluid • Septic thrombi • Infective endocarditis vegetations (on heart valves) Major surgeries (especially hip, knee, abdominal, pelvic) → reduce blood flow → ↑ risk of clots • Prolonged immobility: • Long flights • Sitting for extended periods • Cramped travel conditions
30
What is lung cancer
Sites of metastasis: liver, adrenal, bone, brain Complications: SPHERE: superior vena cava, pancoast tumor, Horner syndrome, endocrine, recurrent laryngeal nerve compression, effusions Squamous cell and small cell carcinomas are often caused by tobacco smoking
31
Small cell carcinomas
Small cell ( oat cell): centrally located, undifferentiated and very aggressive, may cause neurological paraneoplastic syndromes and endocrine paraneoplastic syndromes
32
Non small cell carcinomas
Adenocarcinoma: peripheral location, mutation of KRAS, EGFR and ALK associated w clubbing Squamous cell carcinoma: central location, hilar mass from bronchus, hypercalcemia Large cell carcinomas: peripheral location, highly anaplastic undifferentiated tumor may produce hCG Bronchial carcinoid tumor: central or peripheral, metastasis is rare and we have nest of neuroendocrine cells Pancoast tumor: occurs in apex of lung
33
Staging of lung cancer
T1: tumor less than 3cm w/o pleural or mainstream bronchus T2: tumor 3-5cm with involvement of mainstream bronchus. T3: tumor 5-7cm involves parietal pleura, chest wall, phrenic nerve T4: tumour more than 7cm w invasion of mediastinum, heart etc N0: no metastasis to regional lymph nodes N1: ipsilateral intraparenchymal involvement N2: metastasis to ipsilateral mediastinal lymph nodes N3: metastasis to contralateral mediastinal lymph nodes M0: no metastasis M1: distant metastasis
34
What are the paraneoplastic syndromes in lung cancer
Horners syndrome Superior vena cava syndrome SIADH Eaton lambert syndrome Clinical features: facial and upper extremity swelling, low Ach release
35
What is pulmonary alveolar proteinosis
Abnormal processing of surfactant by macrophages (primary or acquired) • Deposition of amorphous lipoproteinaceous material (phospholipids and surfactant apoproteins)in the alveoli
36
Acute epiglottis
Acute inflammatory condition, confined to supraglottic structures, main cause is haemophillus influenza type B
37
Acute epiglottis vs laryngotracheobronchitis
Acute: H influenza is the cause and we see a thumb sign on x ray Laryngeal: parainfluenza virus is the cause and we see a steeple sign on x ray
38
What is tuberculosis
Infectious granulomatous disease caused by Mycobacterium (acid-fast bacilli) • Forms caseous (cheese-like) granulomas called tubercles, mainly in lungs and lymph nodes • Can affect any organ, commonly: • Lungs, lymph nodes, liver, spleen, pleura, intestines • Symptoms vary depending on the organs involved Transmitted by: infected cattle, they inhale the air, feaces, milk, urine, vaginal and uterine
39
How is tuberculosis spread
Spreads in two stages: 1. Primary complex 2. Postprimary dissemination ⸻ Primary Complex (early stage): • Includes: • Initial lesion at the site of entry (usually lungs via inhalation) • Regional lymph node involvement • Sometimes lesions are only seen in pharyngeal or mesenteric lymph nodes • Primary focus appears within 8 days • Calcification starts by 2 weeks • A tubercle forms: necrotic center surrounded by granulation tissue, monocytes, and plasma cells • Bacteria spread to nearby lymph nodes and cause similar lesions
40
Pulmonary involvement of tuberculosis
Chronic, mild cough (not loud, occurs once or twice at a time) • Triggered by pharynx pressure, exercise, cold, or in the morning • In advanced stages: • Dyspnea (shortness of breath) with rapid, deep breathing • Abnormal chest sounds: • Dullness on percussion • Absent breath sounds in damaged areas • Crackles (squeaky) in affected lung regions • Bronchial lymph node enlargement may: • Compress airways → worsen dyspnea • Cause mediastinal lymph node swelling, linked to persistent ruminal tympany
41
What is the tuberculin test
Involves intradermal injection of bovine PPD (purified protein derivative) • A positive result shows swelling at the injection site after 72 hours, indicating delayed hypersensitivity