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USMLE Step 1 High‐Yield Respiratory/Pulmonology Topics

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Respiratory / Pulmonology

High Yield USMLE Step 1 Notes

Welcome to the Respiratory / Pulmonology High-Yield Notes for Step 1.

These are the most commonly tested topics on the exam—ideal for quick review in your last 2 weeks before the exam, when you’re short on time, or when you’re just starting out and want to focus on what is high yield. Created and peer-reviewed by physicians who scored 260+ on Step 1 in a Q&A style to reinforce active learning.

How to use this file

Read the question ➔ cover the answer ➔ self-quiz before revealing.
Review the NOTES ➔ they include high-yield details you don’t want to miss.
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Embryology

1. A preterm newborn (34 weeks gestation) presents with decreased lung volumes and reduced lung markings on chest X-ray. Pregnancy was complicated by prolonged oligohydramnios. What is the diagnosis?
➔ Pulmonary hypoplasia (↓ Amniotic fluid causes fetal compression → leads to impaired lung development → leads to ↓ alveolar formation)

Note: Pulmonary hypoplasia = Underdeveloped lungs → causes respiratory distress at birth
Bilateral pulmonary hypoplasia → seen in Potter sequence (due to renal agenesis or prolonged oligohydramnios)
Unilateral pulmonary hypoplasia → associated with congenital diaphragmatic hernia (CDH)

2. A neonate born at 32 weeks of gestation develops respiratory distress shortly after birth. Chest X-ray reveals ground-glass opacities and prominent pulmonary vascular markings. What is the diagnosis?
➔ Neonatal Respiratory Distress Syndrome (Occurs in preterm infants due to decreased lung surfactant)

Note: Pathophysiology: ↓ surfactant → leads to ↑ surface tension → causes alveolar collapse (atelectasis) → leading to ↓ compliance, ↓ FRC, ↑ airway resistance
Treatment: antenatal corticosteroids, postnatal surfactant, oxygen support →If not administered surfactant, they develop atelectasis.

3. A congenital failure in the development of the endodermal component of the lung bud is observed. Which function would most likely be impaired?
➔ Surfactant secretion (Endoderm of the lung bud forms type II pneumocytes which is → responsible for surfactant production)

Note: Surfactant Function is to: ↓ Alveolar surface tension → ↑ compliance → prevents atelectasis.
Deficiency → leads to NRDS in preterm infants

4. A pregnant woman presents with premature rupture of membranes at 30 weeks of gestation. What intervention is essential to improve fetal lung maturity and survival?
➔ Dexamethasone (it stimulates surfactant production in premature fetal lungs)

Note: Dexamethasone (a corticosteroid) → ↑ maturation of type II pneumocytes → ↑ surfactant
Insulin inhibits surfactant synthesis → so in infants of diabetic mothers have ↑ risk of developing NRDS

5. A premature infant born at 28 weeks is found to have respiratory distress shortly after birth. Histologic analysis of lung tissue reveals absence of lamellar bodies in alveolar cells. Which cell type is deficient in this patient?
➔ Type II pneumocytes (Type II pneumocytes contain lamellar bodies which store surfactant (dipalmitoylphosphatidylcholine)

Note: Type II pneumocytes also serve as progenitor cells for Type I pneumocytes.

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6. A 1-day-old neonate presents with respiratory distress. Examination reveals decreased breath sounds on the left and bowel sounds in the chest. A chest X-ray shows a feeding tube coiled in the thoracic cavity. What is the diagnosis?
➔ Congenital diaphragmatic hernia (Occurs due to failure of pleuroperitoneal membrane fusion allows abdominal organs to herniate into the thorax)

Note: Neonate + respiratory distress + scaphoid abdomen → think Congenital diaphragmatic hernia
Occurs due to pleuroperitoneal canal failure (Bochdalek hernia). NOT central tendon of diaphragm failure.
Herniation compresses developing lung → leading to pulmonary hypoplasia
Most commonly affects the left side → leading to bowel sounds in the chest

7. A 1-year-old child with a history of neonatal respiratory distress syndrome (NRDS) presents with chronic respiratory symptoms. Chest X-ray shows hyperinflated lungs, flattened diaphragms, diffuse haziness, and coarse linear opacities. What was the risk factor for this condition?
➔ 100% oxygen administration (Prolonged O₂ therapy in neonates causes free radical injury → leading to bronchopulmonary dysplasia)

Note: Caused by prolonged O₂ exposure and mechanical ventilation (Can be a complication of NRDS O2 therapy)
Pathophysiology → hyperoxia → leads to free radical damage → leading to impaired alveolar development and fibrosis
CXR: hazy opacities, overdistended lungs, flattened diaphragm
O2 toxicity can also cause: Retinopathy of prematurity (ROB) and Intraventricular hemorrhage (IVH).

8. A newborn develops cyanosis and respiratory distress that worsens during feeding but improves when crying. An attempt to pass a nasogastric tube fails. What is the diagnosis?
➔ Bilateral choanal atresia (a congenital blockage of both nasal passages)

Note: Caused by failure of posterior nasal passage to canalize
Bilateral form presents at birth with cyanosis relieved by crying (which allows mouth breathing)
It’s associated with inability to pass a Nasogastric Tube.
Often part of CHARGE syndrome: Coloboma, Heart defects, Atresia of choanae, Retardation of growth, GU anomalies, Ear anomalies

Anatomy & Histology

9. A 3-year-old child presents with fever and ear pain. Otoscopy reveals fluid behind an erythematous tympanic membrane. What is the path of infection spread to the middle ear?
➔ Nasopharynx → auditory tube → middle ear (Short, horizontal Eustachian tube in children allows easy bacterial ascent)

Note: Common causing pathogens: Streptococcus pneumoniae, Haemophilus influenzae (nontypeable), Moraxella catarrhalis

10. 40 year old woman presents with RUQ pain referred to her right shoulder. What is the root of referred pain?
➔ C3,C4, C5 (phrenic nerve).It carries diaphragmatic sensory fibers → refers pain to shoulder

Note: Phrenic nerve (C3-C5) innervates the diaphragm.
Irritation of these organs refers pain to the shoulder (through C4 dermatome):
i. Gallbladder/liver → Right shoulder (Kehr’s sign or referred RUQ pain via phrenic).
ii. Splenic rupture/subphrenic abscess → Left shoulder pain (also via phrenic).

11. During cardiac surgery, a nerve running along the pericardium is accidentally injured. Postoperatively, the patient shows paradoxical elevation of the right hemidiaphragm during inspiration. What is the complication?
➔ Diaphragmatic paralysis (Due to phrenic nerve injury → leading to impaired diaphragmatic contraction)

Note: Phrenic nerve (C3-C5) runs along pericardium; damage causes paradoxical diaphragm movement
Paradoxical movement: means paralyzed hemidiaphragm moves upward during inspiration instead of downward.

12. A 60-year-old man with a history of alcoholism presents with fever, cough, and putrid sputum. He was found vomiting while sitting upright. Which lung segment is affected?
➔ Right lower lobe (In an upright position, gravity directs aspirated contents into the right lower lobe)

Note: Upright aspiration → affects Right lower lobe (especially posterior basal segments)
Supine aspiration → affects Right upper lobe (posterior segment) or superior segment of right lower lobe
Risk Factors: altered mental status, anesthesia, seizures, alcoholism, poor dentition.
Organisms involved are Fusobacterium, Peptostreptococcus and Bacteroides.
Treated with Clindamycin (inhibit protein synthesis by binding to 50s and blocking translocation.)

13. A patient with lobar pneumonia caused by Streptococcus pneumoniae is found to have rapid spread of infection between adjacent alveoli. Which of the following lung structures facilitates this process?
➔ Pores of Kohn (Small interalveolar openings that allow spread of organisms and promote collateral ventilation)

14. A patient presents with hypotension and tachycardia after sustaining a stab wound to the right side of the neck, just above the clavicle between the sternum and midclavicular line. Which structure is most likely injured?
➔ Pleura (The lung apex extends into the neck → injury may affect the pleura causing → pneumothorax)

Note: Lung apex extends above the first rib into the root of the neck (Located above medial clavicle, between sternoclavicular joint and midclavicular line)
Injury to lung apex may also:
○ damage the recurrent laryngeal nerve → leading to hoarseness
○ damage the subclavian vessels → leading to upper extremity edema or hemorrhage
○ cause thoracic outlet syndrome.

15. A patient develops a left-sided pleural effusion with a milky appearance and elevated triglyceride levels following neck surgery. What is the most likely cause?
➔ Thoracic duct injury (Injury to thoracic duct causes chylothorax as lymphatic fluid leaks into pleural space)

Note: Milky effusion + ↑ triglycerides → is diagnostic of thoracic duct injury
Thoracic duct drains into left subclavian vein (only in 75% of cases as there are anatomical variations)

16. A patient with obstructive sleep apnea (OSA) is treated with an implantable device that stimulates a nerve in the neck to improve upper airway patency during sleep. Which nerve is targeted by this therapy?
➔ Hypoglossal nerve (Stimulation of CN XII protrudes the tongue to prevent airway obstruction in obstructive sleep apnea)

Note: Obstructive sleep apnea causes hypoxia:
→ results in vasoconstriction of pulmonary vessels → causing Pulmonary hypertension → leading to Cor pulmonale (RV hypertrophy/failure)
→ causes sympathetic and RAAS activation → leading to systemic hypertension
CPAP improves symptoms and lowers BP

17. A researcher is studying the histologic changes that occur along the respiratory tract from the trachea to the alveoli. Which airway component is the last to disappear as the airway branches distally?
➔ Cilia (Cilia persist until the terminal bronchioles and are the last structural element lost)

Note: Cilia Persist into terminal bronchioles then lost before respiratory bronchioles
It is Important for mucociliary clearance
Loss of ciliary function → leads to mucus retention → Occurs in Kartagener syndrome (primary ciliary dyskinesia)

18. A 45-year-old coal miner presents with chronic cough and dyspnea. Imaging shows small nodular opacities in the upper lobes. Which cells clear the inhaled coal dust?
➔ Macrophages (They phagocytose coal particles in the alveoli)

Note: Alveolar macrophages phagocytose inhaled coal dust but → eventually die, releasing cytokines (e.g., TNF-α, IL-1) → leading to fibrosis
Chronic exposure → leads to black pigmentation of the lung (anthracosis) → later developing fibrosis (pneumoconiosis)

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Physiology

19. A 30-year-old man is running a 10K race. He experiences increased heart rate and respiratory rate. What are the expected changes in his mixed venous oxygen content and splanchnic blood flow?
➔ ↓ Mixed venous O₂; ↓ splanchnic blood flow (as active muscles extract more O₂ and blood is redirected away from the gut)

Note: Increased O₂ extraction by exercising muscles → leads to ↓ Mixed venous O₂
Sympathetic stimulation causes α1-mediated vasoconstriction → causes blood to redirect to muscles and skin → leads to ↓ Splanchnic blood flow

Physiological changes during exercise;

Parameter	Change	Explanation
Pulmonary Vascular Resistance (PVR)	↓	Pulmonary vasodilation accommodates increased blood flow.
Hemoglobin Dissociation Curve	→ Right Shift	Increased temperature, CO₂, and H⁺ (Bohr effect) enhance O₂ unloading.
V/Q Ratio	→ More Uniform	Perfusion of lung apices improves, optimizing gas exchange.
Mixed Venous O₂ Content	↓	Tissues extract more O₂ due to higher demand.
Splanchnic Blood Flow	↓	Blood is diverted to active muscles.
Blood pH	↓	Lactic acid production and increased CO₂ cause transient metabolic acidosis.

20. A 60-year-old man with long-standing hypertension is found to have elevated levels of angiotensin II. The enzyme responsible for converting angiotensin I to angiotensin II is primarily produced by which organ?
➔ Lung (ACE is located in pulmonary endothelium and converts Ang I → Ang II)

Note: ACE breaks down bradykinin → so ACE inhibitors ↑ bradykinin → leading to cough, angioedema
Highest concentration of Angiotensin II is present in pulmonary veins

21. A 65-year-old man with ARDS is intubated and placed on mechanical ventilation with a positive end-expiratory pressure (PEEP) of 10 cm H₂O. Which of the following best describes the changes in alveolar pressure, intrapleural pressure, and peak inspiratory pressure?
➔ All increase (PEEP increases intrathoracic pressures across the board)

Note: ↑ PEEP → leads to ↑ intrathoracic pressure → compresses vena cava → leads to ↓ venous return
↑ PEEP → can cause overdistention of alveoli → can be complicated to → pneumothorax

22. In a study, healthy volunteers are exposed to hypoxic conditions, and their alveolar oxygen tension (PAO₂) is experimentally reduced from 120 mmHg to 55 mmHg. Which blood vessels will show an increase in pressure in response to this hypoxia?
➔ Pulmonary blood vessels (As Hypoxia leads to → pulmonary vasoconstriction → redirects blood to better-ventilated alveoli)

Note: In the pulmonary circulation, hypoxia causes vasoconstriction (opposite of systemic circulation).
Chronic hypoxia (e.g., in COPD or high altitude) → ↑ pulmonary vascular resistance → leads to pulmonary hypertension

23. A newborn is evaluated shortly after birth. What happens to pulmonary blood flow within the first few minutes of life?
➔ Increase (Oxygen causes vasodilation → decreases pulmonary vascular resistance → leads to increased pulmonary blood flow)

Note: In pneumonia, inflammation may override this mechanism due to immune-mediated vasodilation and vascular leak.
Local mediators involved in this are : nitric oxide (NO), prostaglandins, TNF-α, and IL-1.

24. A 60-year-old intubated man has a PaCO₂ of 50 mmHg and a PaO₂ of 65 mmHg on mechanical ventilation. Which ventilator adjustment will most effectively lower his PaCO₂?
➔ Increase tidal volume (CO₂ elimination improves with increased minute ventilation, primarily through increasing tidal volume or respiratory rate)

Note: PaCO₂ is inversely related to alveolar ventilation → so increase tidal volume or respiratory rate to lower PaCO₂.
PaO₂ is improved by increasing FiO₂ or PEEP.
Avoid excessive PEEP to prevent barotrauma.
In ARDS, we allow permissive hypercapnia using low tidal volumes to prevent lung injury.

25. A 58-year-old man with a 30-pack-year smoking history is evaluated for chronic cough. Compared to a nonsmoker, which of the following best describes the changes in mucus secretion, ciliary activity, and alveolar macrophage function?
➔ ↑ Mucus secretion, ↓ Ciliary activity, ↓ alveolar macrophage function

Note: Smoking induces goblet cell hyperplasia and impairs both mucociliary clearance and immune defense
Goblet cell hyperplasia + submucosal gland hypertrophy→ leads to ↑ Mucus → leads to chronic bronchitis.
↓ Ciliary activity: Impairs mucociliary clearance → ↑ risk of bronchiectasis.
↓ Macrophage function: ↑ risk of respiratory infections, including tuberculosis.

26. A 25-year-old woman at 20 weeks of gestation has a respiratory rate of 22/min. She has no signs of infection or distress. What best explains her increased respiratory rate?
➔ Respiratory compensation for fetal CO₂ production (Maternal hyperventilation removes excess fetal CO₂ via placental exchange)

Note: Pregnancy increases O₂ demand and CO₂ production → triggers maternal hyperventilation.
This compensates for fetal metabolism by enhancing maternal CO₂ clearance.
In late pregnancy, diaphragm elevation from the enlarging uterus may limit lung expansion, but RR stays elevated due to metabolic drive.

27. A 75-year-old man undergoes routine pulmonary function testing as part of a health evaluation. He has no history of smoking or lung disease. What sets of changes occur in normal aging in terms of Residual volume, PAO2, A-a gradient?
➔ RV ↑, PAO₂ ↓, A–a gradient ↑

Note: Changes with aging:
↑ RV: Due to loss of elastic recoil → leads to air trapping.
↓ PAO₂: Caused by V/Q mismatch and thickened alveolar membranes → reduced diffusion.
↑ A–a gradient: Reflects impaired oxygen transfer despite preserved ventilation.

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Infections / Inflammatory Conditions

28. A 35-year-old man with HIV presents with 3 days of fever, productive cough, and pleuritic chest pain. Temp: 39°C. Lung exam shows crackles and bronchial breath sounds over the right lower lobe. CXR shows lobar consolidation. What is the most likely diagnosis?
➔ Community-acquired pneumonia (S. pneumoniae) (Acute presentation with lobar infiltrate + high fever in HIV suggests → typical bacterial pneumonia, most often due to S. pneumoniae.)

Note: VS Pneumocystis jirovecii pneumonia (PCP) which presents subacutely with low-grade fever, nonproductive cough, and bilateral interstitial infiltrates.
if pneumonia:
→ Acute + lobar + high fever → think S. pneumoniae
→ Subacute + interstitial + hypoxia → think PCP

29. A 19-year-old college student presents with a dry cough, low-grade fever, and fatigue. Temp: 37.9°C. Exam shows scattered crackles without consolidation. Labs reveal Hb 9 g/dL, ↑ reticulocytes, and positive cold agglutinins. What is the most likely diagnosis?
➔ Mycoplasma pneumonia with autoimmune hemolytic anemia (Young adults with atypical pneumonia symptoms + cold agglutinin hemolysis → think Mycoplasma pneumoniae.)

Note: Extrapulmonary findings:
→ Cold agglutinin hemolytic anemia (IgM-mediated leads to → ↑ reticulocytes, ↓ Hb)
→ Erythema multiforme, neurologic symptoms
CXR in CAP: May show:
→ Lobar consolidation → think typical pathogens → as Streptococcus pneumoniae
→ Patchy infiltrates that is more extensive than physical exam → think atypical pathogen → As Mycoplasma pneumoniae (walking pneumonia)
Treated with Macrolides (azithromycin) or doxycycline

30. A 60-year-old man with CHF presents with dyspnea and orthopnea. Vitals are stable. Lung exam reveals decreased breath sounds and stony dullness at the right lung base. What is the most likely diagnosis?
➔ Pleural effusion (transudative) (CHF causes transudative effusion due to increased hydrostatic pressure.)

Note: Transudate effusion is Caused by systemic factors that ↑ hydrostatic or ↓ oncotic pressure → e.g., CHF, cirrhosis, nephrotic syndrome
CXR shows: Blunting of costophrenic angle.
Treat underlying cause (e.g., diuretics for CHF)

31. A 60-year-old patient presents with ascites, lower extremity edema, and bilateral pleural effusion. Echocardiogram shows normal ejection fraction (EF 60%). What is the cause of the pleural effusion?
➔ ↓ Plasma Osmotic Pressure (Cirrhosis leads to low plasma protein, causing reduced plasma osmotic pressure)

Note: Cirrhosis: Causes hypoalbuminemia → ↓ plasma osmotic pressure → fluid leakage (ascites, pleural effusion).
Normal EF (60%) rules out systolic heart failure.
Ruling out Cardiac Cause: Normal BNP and PCWP.

32. A 58-year-old man presents with fever and a productive cough. CXR shows a left-sided pleural effusion. Thoracentesis reveals pleural fluid protein of 4.5 g/dL and LDH of 300 U/L. Serum protein is 6.0 g/dL and serum LDH is 400 U/L. What is the nature of this pleural effusion?
➔ Exudative effusion (Meets Light’s criteria: protein/serum protein > 0.5 and LDH/serum LDH > 0.6.)

Note: Light’s Criteria are used to distinguish exudative vs. transudative pleural effusions based on thoracentesis analysis.

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33. 30 y old patients presented with 2 days of fever, rusty sputum, and chest pain. CXR shows right lower lobe consolidation. What physical exam finding is present?
➔ ↑ Tactile fremitus (Lobar consolidation increases sound transmission → leading to increased tactile fremitus.)

Note: Key physical findings in consolidation:
↑ Tactile fremitus
Bronchial breath sounds
Dullness to percussion
Egophony

Comparison of physical exam finding in common pulmonary conditions

Condition	Tactile Fremitus	Percussion	Breath Sounds	Adventitious Sounds	Special Tests
Pneumonia (consolidation)	↑	Dull	Bronchial	Crackles	↑ Egophony, ↑ Whispered pectoriloquy, ↑ Bronchophony.
Pleural Effusion	↓	Dull	↓/Absent	± Pleural rub	↓ Egophony, ↓ Whispered pectoriloquy.
Pneumothorax	↓	Hyperresonant	↓/Absent	—	↓ Fremitus, ↓ Voice sound.s
Atelectasis	↓	Dull	↓/Absent	—	Trachea → toward affected side
Pulmonary Fibrosis	Normal or ↓	Dull or normal	↓	Fine inspiratory crackles	—

34. A 74-year-old man presents with fever, cough, and foul sputum. Chest X-ray reveals a cavitary lesion with an air-fluid level in the right lung. What enzyme is responsible for the tissue destruction seen in this patient’s lung lesion?
➔ Elastase ( During inflammation → release of Neutrophil enzymes as elastase and MPO are released → causes liquefactive necrosis in lung abscesses.)

Note: Lung abscess often results from aspiration of oropharyngeal contents → commonly involving anaerobic bacteria (e.g., Bacteroides, Fusobacterium).
Empyema (pus in pleura) → is a common complication

35. A 35-year-old man presents with fever, pleuritic chest pain. Oxygen saturation is 88% on room air. Chest exam reveals decreased breath sounds and crackles in the right lower lung field. What is the cause of this patient’s hypoxemia?
➔ Ventilation-perfusion (V/Q) mismatch (In pneumonia, inflammation and fluid in alveoli impair ventilation → leading to V/Q mismatch and hypoxemia)

Note: Pneumonia → causes alveoli being filled with exudate → leads to ventilation ↓ while perfusion remains → causes V/Q mismatch
This is a form of intrapulmonary shunt (blood passes through non-ventilated alveoli).
A-a gradient will be elevated in pneumonia VS normal A-a gradient in cases of hypoventilation or high altitude (↓ inspired O₂).

36. A patient presents with fever, night sweats, and weight loss. Chest X-ray reveals a cavitary lesion in the right upper lobe. What describes the mechanism of tissue injury in this condition?
➔ Type IV (delayed-type) hypersensitivity (symptoms suggestive of Mycobacterium tuberculosis leading to → caseating granuloma formation)

Note: Phases of Immune Response in Tuberculosis-Related Lung Injury;
→ Early phase (first 48 hours): Neutrophil response → leads to liquefactive necrosis.
→ Late phase (weeks): CD4+ Th1 cells → causes macrophage activation →leading to caseating granulomas with Langhans giant cells and central necrosis.

37. A patient undergoes a tuberculin skin test for latent tuberculosis screening. Which immune cells are most predominant at the injection site 48 hours after administration?
➔ Macrophages (Macrophages dominate at 24–48 hours → presenting antigen to CD4+ T cells and initiating the delayed-type (Type IV) hypersensitivity response)

Note: Tuberculin skin test is a Type IV hypersensitivity reaction (cell-mediated).
Timeline of immune response:
i. 0–24h: Neutrophils (innate response).
ii. 24–48h: Macrophages present antigen to T-cells.
iii. 72h: Peak CD4+ Th1 produces IFN-γ → which promotes granuloma formation.

38. A 38-year-old immunosuppressed man presents with a 2-week history of cough and progressive dyspnea. Laboratory testing reveals an elevated serum 1,3 β-D-glucan level. What is the cause of his symptoms?
➔ Fungal infection (β-D-glucan is a component of the fungal cell wall and serves as a nonspecific marker for invasive fungal infections

Note: β-D-glucan is present in the cell walls of many fungi (e.g., Candida, Aspergillus, Pneumocystis jirovecii)

39. 35 y old farmer presents with recurring symptoms of dyspnea and cough. Prior episodes quickly resolved with Corticosteroids and antibiotics. CXR shows bilateral reticulonodular infiltrates. Biopsy shows ill- formed granuloma. What’s the diagnosis?
➔ Hypersensitivity pneumonitis (Caused by repeated inhalation of organic antigens (e.g., moldy hay) → which triggers a hypersensitivity reaction in the lungs)

Note: Chronic exposure can lead to pulmonary fibrosis and irreversible lung damage.

40. A 6-year-old boy recently immigrated from Africa and presents with low-grade fever, mild cough, and fatigue. Chest X-ray shows a small calcified lesion in the lower lobe and ipsilateral hilar lymphadenopathy. What is the diagnosis?
➔ Primary tuberculosis (Patient from endemic area + Ghon focus (calcified lesion) → think primary TB)

Note: Primary TB: Often asymptomatic or mild symptoms (low-grade fever, fatigue, cough)
Classic CXR: Ghon focus (granulomatous lesion) + hilar LAD = Ghon complex
Affects lower/mid lung zones
Common in children, immigrants, and unvaccinated individuals
Can progress (especially in immunocompromised) to miliary or secondary TB

Tuberculosis Pathogenesis

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41. A 45-year-old man with advanced HIV presents with chronic cough, weight loss, and night sweats. Chest imaging reveals cavitary lesions in the upper lung lobes. Which underlying process led to this presentation?
➔ Reactivation of latent TB (Immunosuppression → leads to secondary TB (commonly affects upper lobes due to higher oxygen tension)

Note: Secondary TB: caused by reactivation in upper lobes → leads to fibrocaseous cavitary lesions → contagious
Miliary TB is: caused by Hematogenous spread (especially in immunocompromised) → leading to diffuse symptoms

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Obstructive / Restrictive Diseases

42. A 6-year-old girl with a history of asthma presents with shortness of breath, wheezing, and use of accessory muscles. ABG shows: PaCO₂ 30 mmHg, PaO₂ 60 mmHg, RR 28/min. What is the diagnosis?
➔ Acute asthma exacerbation (Low PaCO₂ reflects hyperventilation in early-stage asthma exacerbation due to tachypnea and CO2 washout)

Note: PCO2 is usually low with acute asthma (due to tachypnea and CO2 washout).
Rising or normalizing PaCO₂ (≥40 mmHg) signals respiratory fatigue → indicates impending respiratory failure → indicates intubatio
Initial treatment includes; Inhaled β₂-agonists (albuterol), systemic corticosteroids, and supplemental O₂

43. A 15 y old boy develops shortness of breath while running but not at rest. Auscultation and CXR are normal. What is the diagnosis?
➔ Exercise-induced asthma. (Shortness of breath triggered by exercise with normal examination and imaging is → characteristic of Exercise-induced asthma)

Note: Triggered by airway dehydration during exercise →leading to mast cell degranulation → causes leukotriene-mediated bronchospasm.
Do methacholine (M3 agonist) challenge if the presentation is unclear.
Treat with inhaled B-2 agonist, leukotriene receptor blockers.

44. A 60-year-old patient presents with progressive shortness of breath. Spirometry shows decreased FEV1/FVC and increased RV/TLC. What are the changes in airway resistance and lung compliance?
➔ ↑ Airway Resistance, ↑ Lung Compliance (These findings are characteristic of obstructive lung disease, such as COPD)

Note: Obstructive Lung Disease (e.g., COPD):
→ Air+way narrowing or obstruction → leads to Increased Airway Resistance
→ Destruction of alveoli → leads to loss of elastic recoil → leads air trapping (↑RV/TLC) → leads to Increased Lung Compliance

Flow volume loops of Obstructive VS restrictive lung diseases

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Comparison of Lung Volume Parameters in Emphysema (Obstructive) vs. Pulmonary Fibrosis (Restrictive)

Lung Volume Parameter	Emphysema (Obstructive)	Pulmonary Fibrosis (Restrictive)
TLC	↑	↓
RV	↑	↓
FRC	↑	↓
FVC	↓	↓
FEV₁	↓	↓
FEV₁/FVC Ratio	↓	↑ or ↔

45. A 70-year-old man presents with chronic dyspnea. Pulmonary function tests reveal a reduced FEV₁/FVC ratio and an increased total lung capacity. DLCO is decreased. What is the diagnosis?
➔ Emphysema (Obstructive pattern with ↓ DLCO)

Note: DLCO (Diffusing capacity of the lung for carbon monoxide) helps differentiate types of lung disease:
Obstructive:
○ ↓ DLCO → think Emphysema (alveolar wall destruction)
○ Normal DLCO → think Chronic bronchitis
Restrictive:
○ ↓ DLCO → think Intrinsic causes (e.g. Pulmonary fibrosis)
○ Normal DLCO → think Extrinsic causes (e.g. Obesity, Neuromuscular disorders)

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46. A 65-year-old man with COPD presents with confusion and lethargy. ABG shows pH 7.30, PaCO₂ 55 mmHg, and HCO₃⁻ 27 mEq/L. What is the primary acid-base disturbance?
➔ Primary respiratory acidosis (due to hypoventilation → CO₂ retention)

Note: COPD → causes chronic hypoventilation → ↑ PaCO₂ → leading to respiratory acidosis
Renal compensation → ↑ HCO₃⁻ (delayed)

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47. A 30-year-old patient presents with daytime somnolence. BMI is 65, Hb is 18.5 g/dL. ABG shows PaCO₂ of 60 mmHg and PaO₂ of 65 mmHg. What is the cause of the patient’s symptoms?
➔ Obesity Hypoventilation Syndrome (Daytime hypercapnia (↑ PaCO₂) and hypoxemia (↓ PaO₂) in a patient with obesity are → diagnostic of obesity Hypoventilation Syndrome)

Note: Obesity Hypoventilation Syndrome has daytime hypercapnia and hypoxemia VS Obstructive Sleep Apnea (OSA) typically has normal daytime ABG values.
Chronic hypoxia → leads to ↑ hypoxia inducing factor (HIF) → leads to ↑ Erythropoietin (EPO) → causes Secondary Polycythemia ↑ Hb

48. A 40-year-old man presents with progressive shortness of breath. He is a non-smoker. Spirometry shows a reduced FEV₁/FVC ratio, and chest CT reveals destruction of interalveolar septa. What is the cause?
➔ Inherited Protease Inhibitor (A1-Antitrypsin) Deficiency (Young, non-smoker patient with emphysema is → highly suggestive of A1-antitrypsin deficiency)

Note: A1-Antitrypsin deficiency Causes panacinar emphysema and liver disease.

49. A 70-year-old coal miner presents with weight loss and progressive shortness of breath. Chest X-ray shows a granuloma. What is the predominant component in the center of the lesion?
➔ Concentric Layers of Collagen (Silicosis causes granulomas characterized by collagen deposition in the center)

Note: The granuloma formation in silicosis is directly caused by the silica particles that are inhaled and deposited in the lungs.
Pathogenesis: Silica impairs phagocytes → ↑ risk of TB infection.
CXR Finding: Eggshell calcifications of hilar lymph nodes (pathognomonic).

50. A 40-year-old woman presents with shortness of breath, painful cold fingers in winter, and heartburn. She has no facial wrinkles. Pulmonary function tests show normal FEV₁ and FVC. What is the most likely pulmonary diagnosis?
➔ Pulmonary Hypertension (Normal PFTs with symptoms of systemic scleroderma suggest pulmonary hypertension due to vascular involvement)

Note: Systemic Scleroderma (Diffuse Cutaneous Systemic Sclerosis):
○ Key Features: Raynaud’s phenomenon, GERD, mask-like facies (late), anti-Scl-70 (+) antibody.
○ Pulmonary manifestation are either:
→ Pulmonary Hypertension: Causes Normal PFTs (vascular disease).
→ Interstitial Lung Disease (Fibrosis): Causes ↓ FEV₁/FVC.

51. A 30-year-old African American woman presents with cough, dyspnea, hepatosplenomegaly, and bilateral hilar lymphadenopathy. What is the most likely finding on biopsy?
➔ Granuloma formation (Symptoms suggestive of sarcoidosis → causes formation noncaseating granulomas)

Note: Common features:
○ Bilateral hilar lymphadenopathy
○ Pulmonary symptoms (dyspnea, dry cough)
○ Skin lesions (erythema nodosum) → referred to as painful bumps in the lower extremities
Labs: ↑ ACE levels and , hypercalcemia (due to macrophage 1α-hydroxylase activity)

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Respiratory Neoplasms

Lung Cancer Types:

Type	Location	Key Features	Markers/Histology
Small Cell Lung Cancer (SCLC)	Central	Aggressive, poor prognosis, paraneoplastic syndromes (SIADH, Cushing’s)	Chromogranin A (+), Synaptophysin (+), Neuron-Specific Enolase (+)
Adenocarcinoma	Peripheral	Most common in females, associated with clubbing (hypertrophic osteoarthropathy)	Mucin (+)
Squamous Cell Carcinoma	Central	Bronchial compression → recurrent pneumonia, hypercalcemia (PTHrP), Asbestos exposure: SCC > Mesothelioma	Keratin pearls, intercellular bridges
Carcinoid Tumor	Variable	Produces serotonin → flushing, diarrhea, wheezing (Carcinoid Syndrome)	Chromogranin A (+)
Pancoast Tumor (Superior Sulcus Tumor)	Apex	Compresses regional structures, causing unilateral symptoms: Shoulder pain, atrophy (brachial plexus); UE swelling (brachiocephalic vein); Horner’s syndrome (miosis, ptosis, anhidrosis); Hoarseness (recurrent laryngeal nerve); Hemidiaphragm paralysis (phrenic nerve)	N/A
SVC Syndrome	Mediastinum (due to tumor/thrombus)	Bilateral UE swelling (SVC), Neck swelling, JVD, ↑ Intracranial pressure → dizziness, aneurysm	N/A

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52. A 65-year-old man with a 15-year history of working in shipyards presents for evaluation. He has no significant smoking history. What is the most common cancer associated with his occupational exposure?
➔ Bronchogenic carcinoma of the lung (working in shipyards → causes Asbestos exposure which → increases the risk of Bronchogenic carcinoma

Note: Asbestos Exposure → ↑Risk of Bronchogenic carcinoma more commonly than mesothelioma (which require pleural exposure)

53. A 45-year-old woman with newly diagnosed lung cancer presents with confusion. She reports a history of flank pain a few months ago. Labs show markedly elevated serum calcium. What is the most likely diagnosis?
➔ Hypercalcemic crisis from PTHrP (SCC causes release of → PTHrP → leading to severe hypercalcemia and its complications)

Note: Other causes of hypercalcemia in malignancy:
→ Multiple myeloma: cytokine-induced bone resorption
→Sarcoidosis: ↑1-alpha hydroxylase in macrophages → ↑vitamin D
→ Primary hyperparathyroidism: ↑PTH, not PTHrP
Renal cell carcinoma: May also cause paraneoplastic hypercalcemia, but typically with elevated EPO and hematuria

54. A 63-year-old man presents with progressive weight loss, skin hyperpigmentation, and muscle wasting. Labs show elevated cortisol and ACTH levels. High-dose dexamethasone fails to suppress cortisol production. What is the diagnosis?
➔ Small cell lung cancer (Ectopic ACTH production from SCLC causes → Cushing’s syndrome that is unresponsive to dexamethasone suppression)

Note: Small cell lung cancer→ secretes ectopic ACTH → → causes bilateral adrenal hyperplasia → ↑ cortisol
Cushing syndrome is associated with weight loss if it’s associated with cancer. Otherwise, Cushing causes weight gain.
High-dose dexamethasone suppression test:
→ fails to suppress cortisol in → ectopic ACTH (e.g., SCLC)
→ Suppresses cortisol in Cushing disease (pituitary ACTH overproduction)
Other Associated paraneoplastic syndromes:
– Lambert-Eaton Myasthenic Syndrome (LEMS): autoantibodies against presynaptic Ca²⁺ channels → proximal muscle weakness that improves with use
– SIADH (↑ADH secretion) → causes hyponatremia

55. A 60-year-old man presents with left-sided motor weakness. MRI reveals a solitary brain mass. Biopsy shows small blue cells that are positive for chromogranin and synaptophysin. What is the diagnosis?
➔ Metastatic brain tumor (from small cell lung cancer)

Note: Small blue cells with neuroendocrine markers like chromogranin and synaptophysin is seen in → Small cell lung carcinoma

56. A Chinese patient presents with 5 months of nasal discharge and cervical lymphadenopathy. Biopsy of a nasopharyngeal mass reveals tumor cells positive for Epstein-Barr virus (EBV). Which cell type is primarily infected?
➔ Nasopharyngeal epithelium (EBV is associated with nasopharyngeal carcinoma, especially in Asian populations, and infects respiratory epithelial cells)

Note: Chinese/Southeast Asian ethnicity → ↑ increases the risk
EBV loves respiratory epithelium (Nasopharynx) VS HPV loves squamous epithelium (e.g., Oropharynx, true vocal cords)

57. A 50-year-old patient presents with facial flushing, wheezing, and chronic diarrhea. Imaging reveals a central mass in the right lung. Urinary 5-HIAA levels are elevated. What is the most likely diagnosis?
➔ Carcinoid tumor (facial flushing + wheezing + chronic diarrhea + ↑ 5-HIAA levels → think carcinoid syndrome →caused by Carcinoid tumor)

Note: Bronchial carcinoids secrete serotonin directly into systemic circulation → causing carcinoid syndrome VS GI carcinoids which have to metastasis to the liver first to causes symptoms
Serotonin affects the right side of the heart
→ tricuspid regurgitation, pulmonic stenosis
→ Left-sided valves spared due to serotonin degradation in pulmonary circulation

58. A 42-year-old man presents with progressive proximal lower limb weakness. Reflexes are decreased. Chest X-ray reveals a central lung mass. What part of the neuromuscular junction is targeted?
➔ Presynaptic calcium channel (Symptoms suggestive of Lambert-Eaton myasthenic syndrome which is caused by → Presynaptic autoantibodies targeting calcium channels)

Note: Lambert-Eaton myasthenic syndrome is associated with small cell lung cancer. (paraneoplastic)
Lambert-Eaton Myasthenic Syndrome (LEMS) is associated with proximal muscle weakness + decreased or absent reflexes.
VS Myasthenia Gravis (MG) typically presents with ocular (ptosis, diplopia) and bulbar (dysphagia, dysarthria) muscle weakness, with normal reflexes.

59. A 52-year-old man with a history of smoking presents for routine evaluation. Chest X-ray reveals a solitary “coin lesion.” Biopsy shows mature cartilage mixed with connective tissue. What is the diagnosis?
➔ Hamartoma (Presence of disorganized but mature cartilage and connective tissue indicates → a lung hamartoma)

Note: Most common benign lung tumor in adults.
It originates from Mesenchymal origin which contains cartilage, fat, and fibrous tissue.
No malignant potential — usually found incidentally.
High-yield hamartomas:
→ Lung hamartoma
→ Peutz-Jeghers syndrome (GI hamartomatous polyps + mucocutaneous pigmentation)
→ Tuberous sclerosis (brain and skin hamartomas, renal angiomyolipoma)

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Respiratory Pathologies (Other)

60. A 28-year-old woman presents with sudden-onset pleuritic chest pain, dyspnea, and hemoptysis. Pulse is 120/min, RR is 28/min. CXR shows a mild left basal pleural effusion. What is the most likely diagnosis?
➔ Pulmonary embolism (Sudden-onset dyspnea + pleuritic chest pain + hemoptysis with minimal CXR findings → think PE.)

Note: Low-grade fever (e.g., 38°C) may occur
CXR: Often normal or shows mild findings (e.g., small pleural effusion)
Risk factors (Virchow’s Triad):
○ Stasis: Immobility, long travel, CHF
○ Hypercoagulability: OCPs, pregnancy, cancer, Factor V Leiden
○ Endothelial injury: Trauma, surgery

61. A 48-year-old man with acute pancreatitis develops worsening shortness of breath two days later. He is found to have bilateral crackles and a PaO₂ of 55 mm Hg on 100% oxygen. He is intubated and started on mechanical ventilation. Increasing PEEP helps prevent which complication?
➔ Absorption atelectasis PEEP prevents alveolar collapse by maintaining positive pressure during expiration.

Note: → ARDS can be caused by Pancreatitis, sepsis, aspiration, trauma
→ ARDS → leads to ↑Capillary permeability → leading to albumin deposition → leads to formation of hyaline membranes → impairs gas exchange
→ In ARDS CXR shows Bilateral pulmonary infiltrates (diffuse, patchy, or confluent opacities) VS Pulmonary contusion which causes focal alveolar infiltrates (e.g. Unilateral) after trauma

62. A 25-year-old man with a history of asthma presents with shortness of breath. Vital signs: BP 90/60 mmHg, pulse 120/min, PaO₂ is 50 mmHg. On exams, breath sounds are decreased on the left side. What is the diagnosis?
➔ Tension pneumothorax (Hypotension, hypoxemia, and unilateral ↓ breath sounds point to tension pneumothorax)

Note: Tracheal deviation (to the other side) + neck vein distension confirm → diagnosis.
Requires immediate needle decompression in 2nd intercostal space, midclavicular line

63. A 65-year-old man with a history of COPD presents with sudden-onset shortness of breath and chest pain. Vitals: BP 100/65 mmHg, pulse 110/min, SpO₂ 88% on room air. Exam shows ↓ breath sounds and hyperresonance on the right side. What is the diagnosis?
➔ Secondary spontaneous pneumothorax (Rupture of emphysematous bullae in COPD leads to → air in the pleural space)

Note: Management: High-flow oxygen + large-bore chest tube if symptomatic or large pneumothorax

64. A 20-year-old man presents with shortness of breath and chest pain that worsens with deep inspiration after a motor vehicle accident. What finding indicates a rib fracture?
➔ Subcutaneous crepitus ( Rib fracture with lung injury → causes Air escaping from the lung into soft tissue)

Note: In severe cases, flail chest may occur, characterized by paradoxical chest wall movement during respiration.

65. A 45-year-old male presents to the emergency department after a motor vehicle accident. He is hypotensive, with a blood pressure of 80/50 mmHg, muffled heart sounds, and distended neck veins. What is the diagnosis?
➔ Cardiac tamponade ( hypotension + JVD + muffled heart sounds → indicates Beck’s triad → which is classic for tamponade)

Note: Pulsus paradoxus(which is >10 mmHg drop in SBP with inspiration) is → supportive finding
Diagnosis Confirmed with echocardiogram
Key differentiator:
→ cardiac tamponade causes → Clear lungs on auscultation → suggests the issue is primarily related to pericardial compression
→ VS congestive heart failure (CHF) causes → rales or crackles on auscultation → suggests pulmonary edema → as fluid backs up into the lungs due to heart failure.

Treated with Immediate pericardiocentesis

66. A 3 year old boy suddenly develops coughing and wheezing while playing with small toy. examination shows Unilateral decreased breath sounds. What is the diagnosis?
➔ Foreign body aspiration (Commonly aspirated into the right main bronchus due to its wider and more vertical orientation)

Note: CXR may show hyperinflation on one side (ball-valve effect).
Rigid bronchoscopy is diagnostic and therapeutic for foreign body removal.

67. A 19-year-old woman is stung by a bee and rapidly develops shortness of breath, hypotension, urticaria, and wheezing. What is the most likely diagnosis?
➔ Anaphylactic shock (Type I hypersensitivity reaction) (Mast cell degranulation leads to histamine release → causing vascular leak and bronchospasm)

Note: First-line treatment: IM epinephrine.
Also administer antihistamines, steroids, and fluids.
Airway management is crucial — intubation may be required in severe cases.

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Pharmacology

68. A 28-year-old woman with a history of severe asthma presents to the ER with an exacerbation. After receiving multiple doses of albuterol. What is the most likely side effect?
➔ Tremors (β2-agonist overstimulation causes skeletal muscle tremors)

Note: β2-agonist Toxicity may lead to Tachycardia and hypokalemia with excessive use.

69. A 35-year-old man with asthma is prescribed a leukotriene receptor blocker as part of his management plan. What type of receptor does this medication target?
➔ G protein-coupled receptor (It targets the Gq-coupled CysLT1 receptor, blocking leukotriene D4 to reduce bronchoconstriction and inflammation)

Note: Used in Asthma prophylaxis ( not for acute exacerbations).

70. A patient with COPD is started on a new medication that leads to decreased salivation and mucus production. What is the mechanism of action of this drug?
➔ Muscarinic antagonist (it Blocks M3 receptors in the airways leads to → reducing bronchial secretions and smooth muscle contraction)

Note: Used as First-line treatment in COPD (also used as an adjunct treatment in asthma)

71. A 68-year-old man with advanced COPD is being treated with theophylline. He was recently prescribed fluconazole for a fungal infection. A few days later, he developed tremors and palpitations. What is responsible for these symptoms?
➔ Inhibition of the P450 system (Fluconazole inhibits CYP450, leading to elevated theophylline levels and toxicity)

Note: Theophylline has a narrow therapeutic index.
P450 inhibitors (e.g., fluconazole, clarithromycin, cimetidine) can raise serum theophylline levels.
Another common scenario is a patient with multidrug resistance COPD developing → seizure or palpitations .

72. A 20-year-old woman with pulmonary arterial hypertension is started on a medication that enhances pulmonary blood flow by preventing degradation of a messenger involved in smooth muscle relaxation. Which medication is she most likely taking?
➔ Sildenafil (Prevents cGMP breakdown via PDE-5 inhibition → promoting pulmonary vasodilation)

Note: Contraindicated with Concurrent nitrate use → due to risk of severe hypotension

73. A 30-year-old woman with pulmonary arterial hypertension started on bosentan. What is the mechanism of action of this medication?
➔ Endothelin receptor blocker (Bosentan blocks endothelin-1 receptors → leading to reducing vasoconstriction and pulmonary vascular resistance)

Note: Endothelin is a potent vasoconstrictor.
Bosentan blocks endothelin-1 receptors VS Epoprostenol which is a PGI2 analogue that induce pulmonary vasodilation.

74. A 50-year-old man presents with 24 hours of high fever, cough, and body aches. He was started on oseltamivir. Which step in the viral life cycle is inhibited by this medication?
➔ Virus release from infected cells (Oseltamivir inhibits neuraminidase → preventing viral progeny from being released)

Note: Oseltamivir is Used for inInfluenza A and B but must be started within 48 hours of symptom onset.
There are two key proteins on influenza virus;
→ Hemaglutinin (HA) → permits virus entry (HA = Helps Attach)
→ Neuraminidase (NA) permits virus release (NA = Necessary for egress (exit)

75. A 45-year-old man with a history of asthma develops nasal polyps and bronchospasms after taking aspirin for mild pain relief. What enzyme is most likely inhibited by aspirin in this patient?
➔ Cyclooxygenase (COX) (Aspirin inhibits COX → leading to decreased production of PGE and TXA2)

Note: Asthma + nasal polyps + aspirin intolerance –. think Aspirin induced asthma
COX inhibition shifts arachidonic acid metabolism towards →
○ Increased leukotriene production → causes bronchoconstriction
○ Reduced PGE₂ (a molecule that normally provides protection to the airways)

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Disclaimer

Version 1.0 May 2025. No part of this document may be reproduced or distributed without written permission. For personal study only. Medical information herein is for educational purposes and does not constitute clinical advice. Always confirm with current guidelines and your institution’s policies.

Prefer a narrative review instead of Q&A style? Scroll down to the section below for high-yield concepts in paragraph format (they cover the same concepts).

Narrative Format

High-Yield Respiratory / Pulmonology Topics

Master USMLE Step 1 Pulmonology/Respiratory with these high-yield notes! Focus on the most tested topics, key pathophysiology, and must-know facts to boost your score.

Embryology
○ Pulmonary hypoplasia
Anatomy & Histology
○ Type of Epithelium
○ IMPORTANT LEVELS
○ Intercostal Nerve Block
Physiology
○ Fibrosis Vs Emphysema
○ High Yield Concepts
○ Acid Base Disorders
○ Oxygen Hemoglobin Dissociation Curve
○ SIDE NOTES
Pathology
○ Flow Volume Loop
○ Obstructive lung disease Vs restrictive lung disease
○ Cystic Fibrosis vs. Kartagener Syndrome
○ DVT/PE
TUMORS
○ Tumors of Head & Neck
○ Mediastinal tumors
○ LUNG AND PLEURAL TUMORS
○ Pleural tumors
○ Classic chest X-rays in Acute Emergencies
○ Type of atelectasis
○ Patient Positioning and Clinical Indications
○ High Yield facts in children
○ Pleural effusions
○ Pneumonia
○ Most common organisms
○ High yield pulmonary fungal infections
○ Pathogenesis
○ Sarcoidosis
○ Tuberculosis
Treatments
○ Pulmonary hypertension medications

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Embryology

Developmental stage.

1. Embryonic
2. pseudoglandular
3. Canalicular: Surfactant formation (By Type II Pneumocytes) begins at this stage. Failure→ pulmonary hypoplasia.

NOTE. Neonatal Respiratory Distress Syndrome (NRDS)

↓ Surfactant → ↑ alveolar surface tension → alveolar collapse (“ground-glass” CXR).

Risk factors:

Prematurity (surfactant starts at 20w, mature by 35w).
Maternal diabetes (↑ fetal insulin → ↓ surfactant synthesis).
C-section delivery (↓ fetal stress → ↓ glucocorticoid surge).

Complications:

Persistently low O₂ → PDA.
Therapeutic O₂ → ROP, IVH, BPD (Retinopathy of Prematurity, Intraventricular Hemorrhage, Bronchopulmonary Dysplasia).
Diagnosis: Lecithin: Sphingomyelin (L:S) ratio < 2 → risk of NRDS.
Treatment: Maternal steroids before birth, exogenous surfactant for newborns.

NOTE. NRDS: ↓ compliance, ↓FRC, ↑ airway resistance.

Saccular (week 26 – Birth): forms saccules (primary septation)
Alveolar (Week 36 – 8 years): forms definitive true sacs (secondary septation).

How is it tested?

Which stage is associated with the beginning of surfactant production? Canalicular phase

Pulmonary hypoplasia

Unilateral: due to congenital diaphragmatic hernia (↓ breath sound on the left side, bowel sound in the left chest)

Bilateral: Potter sequence (associated with bilateral renal agenesis)

Prolonged 100% O2 Therapy → bronchopulmonary dysplasia, retinopathy of prematurity, and Intraventricular hemorrhage (IVH).

-Tracheoesophageal fistula: incomplete separation of the foregut into the trachea and esophagus. The most common variant is TEF with esophageal atresia, where the proximal esophagus ends in a blind pouch while the distal esophagus remains connected to the trachea. Presents with Choking, drooling, coughing, and regurgitation with first feed. Air in the stomach—inability to pass an NG tube.

-Bilateral Choanal atresia: Respiratory distress and cyanosis worsened by feeding, relieved by crying.

Anatomy & Histology

Type of Epithelium

Pleura: Visceral (NOT sensitive) and Parietal (Sensitive).

– innervation of parietal pleura:

–Phrenic nerve (C3, C4, C5): mediastinal and diaphragmatic pleura. Pain is radiated to the shoulder and neck.

– Intercostal nerve: intercostal pleura.

How is it tested? A 40-year-old woman presents with RUQ pain referred to her right shoulder. What are the roots of the nerve? A: Phrenic (C3, C4, C5)

Lungs:
Injury of apex of lung.

How is that tested? A patient developed a knife stab to the Rt chest above the medial side of Rt clavicle and just lateral to manubrium sterni, which structure is most likely injured? Lung

Bronchi: The right side is shorter, wider, vertical than the left.
Right bronchus is the common site of aspiration (foreign body, aspiration pneumonia)

NOTE. Aspiration: lower lung zones→ if the patient is upright upper lung zones→if the patient is supine

Particle size and mode of clearance: Large (≥ 10 μm): Nasal Cavity, Medium (3–10 μm): Trachea, Bronchi (Mucociliary clearance), Small (< 3 μm): Alveoli (Alveolar Macrophages).

How is it tested? A 45-year-old patient presents with dyspnea and cough for the past few months. He works in a mine. The small particles of coal are cleared by which cells? : Macrophages

IMPORTANT LEVELS

Surface Anatomy of Organs in Relation to Rib Levels:

Liver Upper Border: 5th rib (midclavicular), 7th rib (midaxillary), 9th rib (paravertebral). Risk of liver damage during expiration
Lung Lower Border: 6th rib (midclavicular), 8th rib (midaxillary), 10th rib (paravertebral)
Pleura Lower Border (2 levels below lung): 8th rib (midclavicular), 10th rib (midaxillary), 12th rib (paravertebral).

How is it tested? A patient developed a knife stab to the right chest between ribs 6 and 7 in the midclavicular line. Which structure is most likely injured? Liver

-Chest tube placement→ 4th or 5th intercostal space, anterior or mid-axillary line (Serratus anterior is penetrated). What’s the most common location of chest tube placement?

-Needle decompression→2nd intercostal space midclavicular or 4th, 5th intercostal space, anterior or mid-axillary line.

Intercostal nerve block

Intercostal nerve block: To avoid injury to intercostal vessels (VAN—Vein, Artery, Nerve) running in the costal groove, injection should be administered near the upper border of the lower rib, rather than the lower border of the target rib.

– Structures perforating the diaphragm.

T8: IVC, T10: Oesophagus (and vagus), T12: Aorta ( with Azygus, thoracic duct, phrenic nerve).

Nerves & Muscles USED FOR RESPIRATION:

Inspiration: Under basal condition→Diaphragm, supplied by phrenic nerve (C3, C4, C5)

In distres→scalene muscles, Sternocleidomastoid (CN IX) and external intercostal.

Expiration: Usually passive with relaxation of Diaphragm.

Active expiration→internal intercostal, abdominal muscles.

How is it tested? A patient developed trauma to spinal roots C3, C4, C5. What is the effect on Maximal inspiratory and expiratory pressure? In case of phrenic nerve injury, Maximum inspiratory pressure is decreased (dependent on diaphragm), while Maximum expiratory pressure is normal (dependent on abdominal, intercostal muscles).

– Important cranial nerves related to respiration

CN X: –Damage to the recurrent laryngeal nerve results in hoarseness of voice airway obstruction.

CN IX: supplies sternocleidomastoid(SCM) used during active inspiration.

CN XII: hypoglossal nerve stimulator can be used in obstructive sleep apnea.

Physiology

Fibrosis Vs Emphysema

Lung Volume Parameter	Emphysema (Obstructive)	Pulmonary Fibrosis (Restrictive)
TLC	↑	↓
RV	↑	↓
FRC	↑	↓
FVC	↓	↓
FEV₁	↓	↓
FEV₁/FVC Ratio	↓	↑ or ↔

How is it tested? A patient with a 2-month history of dyspnea and cough. Auscultation shows bilateral fine crackles. Which of the following is increased? A: FEV1/FVC

High Yield concepts

–Functional residual capacity(FRC): The point where the collapsing force of the lungs =the expanding force of the chest wall is the resting equilibrium of the respiratory system = Zero.

–Elastic recoil: Tendency to collapse (High in fibrosis and low in emphysema).

–Compliance: change in volume for a change in pressure. If less pressure is required to inflate the lung, the higher compliance it has. E.g. Fibrosis needs much pressure to inflate the lung, so low compliance.

–Expiratory flow rate → ↑in fibrosis due to enhanced radial traction on the bronchioles from fibrotic lung tissue and ↓ in emphysema due to reduced radial traction, resulting from alveolar wall destruction.

Ventilation/ perfusion Mismatch.

-Oxygen supplementation typically improves dead (PE) space but not shunt (Atelectasis)

– In exercise→Pulmonary capacity (ventilation) exceeds cardiac output(Perfusion) ↑V/Q ratio

Central & peripheral chemoreceptors.

Central: in the medulla. Responds to ↑CO2.

Peripheral: Aortic Arch(Vago-vagal) and Carotid Body (Glossopharyngeal- vagal). Responds to changes in CO2, pH, and O2.

-Patients with COPD often experience chronic hypercapni→desensitization of central chemoreceptors to CO2→ primary respiratory drive shifts to hypoxemia. Administering 100% oxygen→suppress this hypoxic drive→ respiratory depression.

How is it tested? A COPD patient developed resp distress, after administering 100% he became confused and ABG finding showed elevated PaCO2. The reason is suppressing peripheral chemoreceptors.

Condition	PaO₂	SaO₂	Oxygen Content
CO Poisoning	N	↓	↓
Cyanide Poisoning	N	N	N
Anemia (↓ Hb)	N	N	↓
Polycythemia (↑ Hb)	N	N	↑
High Altitude	↓	↓	↓

How is tested? A patient is exposed to fires.

Carbon monoxide is detected in blood.

What the changes in PaO2, SaO2, and oxygen content?

-Cyanide→ impairs electron transport chain Type IV; it’s characterized by ↑venous oxygen content (↓ consumption of O2 by peripheral tissues).reversed with Hydroxycobolamin (forms Cyanocobalamin) or Nitrites (induce Meth hemoglobin) and Sodium Thiosulfate (forms sodium thiocyanate

-High altitude and hypoventilation (The 2Hs)→Normal A-a gradient (dec PAO2, dec PaO2, dec O2 content).

How is it tested?

Acid-Base disorders

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How is it tested? What’s the acid-base balance in the following conditions?

-Emphysema, Asthmatic Attack (Severe), Myasthenia Gravis, Pneumonia, Pneumothorax: ↓pH, ↑PCO2, ↑HCO3

-Pulmonary Fibrosis, Pulmonary Embolism, Pregnancy, High Altitude, Early Salicylate Poisoning: ↑pH, ↓PCO2, ↓HCO3

Oxygen Hemoglobin Dissociation Curve

–left shift (↑ affinity of Hb to O2): ↓ in CO2, 2,3 BPG, Temp, H+ (High pH)

–Right shift: (↓ affinity of Hb to O2) ↑ CO2, 2,3 BPG, Temp, H+ (High pH)

-2,3-BPG ↑at high altitudes to reduce hemoglobin’s affinity for oxygen, thereby enhancing oxygen release at the tissue level.

– Fetal Hemoglobin (HbF): Causes a left shift in the oxygen dissociation curve due to higher O₂ affinity, facilitating oxygen transfer from maternal blood.

–Methemoglobin (MetHb): causes a left shift but with reduced O₂-carrying capacity due to the oxidation of Fe²⁺ to Fe³⁺. Causes cyanosis of lips and mucous membranes. Risk factors include nitrites, and benzocaine. Treated with methylene blue.

– Carbon monoxide(CO): Associated with left shift. Causes headaches and flushing. Risk factors include fumes, fires. Treated with 100% O2

-Hemoglobin exhibits positive cooperativity, resulting in a sigmoidal oxygen dissociation curve. In contrast, myoglobin has a single subunit, lacks cooperativity, and follows a hyperbolic oxygen dissociation curve, reflecting its role as an efficient O₂ storage protein rather than a transporter.

– Airway resistance: is highest in the segmental bronchi and lowest in the terminal bronchioles.

Pulmonary function tests with normal aging

↑: V/Q mismatch, FRC, RV, A-a gradient, ↓: PaO2, FEV1, FVC, ↔: TLC

-In elderly: Elastin ↓ (↑ compliance) and chest wall gets stiffer (↓ compliance). Overall compliance is ↓ .

Haldane effect (peripheral tissue):

CO₂ is converted into HCO₃⁻ and H⁺, with H⁺ binding to hemoglobin (Hb). To maintain electrochemical balance, HCO₃⁻ exits RBCs in exchange for Cl⁻ (chloride shift). As a result, venous blood has a higher Cl⁻ content compared to arterial blood.

Bohr effect (Lung). H⁺ binds with HCO₃⁻ to form CO₂, which is then exhaled. To maintain electrochemical balance, Cl⁻ exits RBCs as HCO₃⁻ re-enters (reverse chloride shift). As a result, arterial blood has a lower Cl⁻ content compared to venous blood.

How is it tested? Inside RBC, Which ion has a higher concentration in venous blood compared to arterial blood? A: Chloride

Response to high altitude:

Parameter	Change	Explanation
PaO₂	↓	Lower atmospheric O₂ reduces arterial O₂ levels.
PAO₂	↓	Decreased atmospheric O₂ lowers alveolar O₂.
A-a Gradient	Normal	Both PAO₂ and PaO₂ decrease proportionally, keeping the gradient unchanged.
HCO₃⁻	↓	Renal compensation for respiratory alkalosis (excretes HCO₃⁻ to lower pH).
pH	↑	Hypoxia-induced hyperventilation causes respiratory alkalosis.
2,3-BPG	↑	Increases to enhance O₂ unloading from hemoglobin to tissues.
Erythropoiesis	↑	Hypoxia stimulates EPO release, increasing RBC production for better O₂ delivery.
Acetazolamide Effect	↑	Carbonic anhydrase inhibition increases HCO₃⁻ excretion, speeding up pH normalization and acclimatization.

NOTE. Prolonged exposure to high altitude ↑the risk of right ventricular hypertrophy due to persistent pulmonary hypertension. Uneven hypoxic pulmonary vasoconstriction→ high-altitude pulmonary edema (HAPE), which occurs despite a normal pulmonary capillary wedge pressure (PCWP).

Response to Exercise:

Parameter	Change	Explanation
Pulmonary Vascular Resistance (PVR)	↓	Pulmonary vasodilation accommodates increased blood flow.
Hemoglobin Dissociation Curve	→ Right Shift	Increased temperature, CO₂, and H⁺ (Bohr effect) enhance O₂ unloading.
V/Q Ratio	→ More Uniform	Perfusion of lung apices improves, optimizing gas exchange.
Mixed Venous O₂ Content	↓	Tissues extract more O₂ due to higher demand.
Splanchnic Blood Flow	↓	Blood is diverted to active muscles.
Blood pH	↓	Lactic acid production and increased CO₂ cause transient metabolic acidosis.

SIDE NOTES

– Exercise: Mixed venous O₂ is ↓ due to ↑tissue O₂ consumption.

– Heart Failure: Mixed venous O₂ is ↓ as hypoxic tissues extract more O₂ due to inadequate perfusion.

– Sepsis: Mixed venous O₂ is ↑due to impaired tissue O₂ extraction from mitochondrial dysfunction and shunting.

– Cyanide Toxicity: Mixed venous O₂ is ↑as Complex IV inhibition in the electron transport chain prevents O₂ utilization.

Pathology

Flow-volume Loop

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Obstructive lung disease Vs restrictive lung disease

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How is it tested? Arrows questions. For example, which of the following increases in emphysema?

NOTE. – Pulmonary arterial hypertension (PAH) and pulmonary fibrosis can be associated with scleroderma. PAH presents with normal pulmonary function tests (PFTs), while fibrosis shows a restrictive pattern.

-Early-onset emphysema (e.g., before age 40) suggests α-1 antitrypsin deficiency, characterized by predominant lower lobe emphysema and hepatomegaly.

Developing asthma after aspirin use suggests aspirin-exacerbated respiratory disease (AERD), caused by excess leukotriene production.

Cystic fibrosis: Autosomal recessive. The most common cause: is ΔF508 mutation→ misfolding of the CFTR protein, preventing it from reaching the cell membrane.

-In the respiratory and GI tract, Cl⁻ secretion is impaired, and Na⁺ reabsorption is uninhibited→ thick, dehydrated mucus due to low Na⁺ and Cl⁻ content.

-In the sweat glands, it’s salty sweat that is rich in Na⁺ and Cl⁻.

Diagnosis: Immunoreactive Trypsinogen– Newborn screening, Sweat Chloride Test – Gold standard, Nasal Potential, Stool Elastase – Evaluates pancreatic insufficiency.

Cystic Fibrosis vs. Kartagener Syndrome

Feature	Cystic Fibrosis (CF)	Kartagener Syndrome (Primary Ciliary Dyskinesia)
Cause	ΔF508 mutation in CFTR, leading to viscid mucus	Defective dynein arm, leading to immotile cilia
Respiratory Infections	*Due to thick mucus and bacterial colonization (Staph aureus* in children, Pseudomonas & B. cepacia in adults)**	Due to impaired mucociliary clearance
Infertility	Due to congenital bilateral absence of the vas deferens (CBAVD)	Due to immotile sperm (dynein defect)
Other Features	Pancreatic insufficiency, salty sweat (high Cl⁻ and Na⁺)	Situs inversus, bronchiectasis, chronic sinusitis

DVT/PE

Risk factors: Tumor (coagulopathy), Long flights (blood stasis), Endothelial damage (e.g. smoking, homocystinuria)

-DVT is common in distal to proximal veins (Popliteal > femoral > iliac) while in PE, the clots commonly come from proximal to distal veins (Popliteal < femoral < iliac)

Manifestations: Unilateral leg swelling, pain and tenderness

– D-dimer is highly sensitive. It’s used to rule out DVT/PE in patients with low risk. A negative test rules out DVT/PE while a positive test is NON-specific for many diseases.

– Ultrasound is used to diagnose patients with moderate-high risk of DVT while CT angio is used to diagnose PE.

– PE commonly occurs due to DVT.

Other causes include:

-Fat embolism (24-72 hours after trauma or bone surgery): Altered mental status, petechial rash, and hypoxemia.

-Amniotic fluid: during labor or postpartum. Worse prognosis.

Acute PE causes dilation of the chamber of right ventricle. While chronic PE causes right ventricular hypertrophy.

-The presence of hemodynamic instability (SBP <90) indicated a worse prognosis.

Manifestations: sudden dyspnea, pleuritic chest pain, Tachycardia, Tachypnea.

– Pulmonary embolism (PE) is typically associated with a clear chest X-ray. Therefore, the presence of clinical manifestations such as acute onset of dyspnea, tachycardia, or hypoxia despite a normal chest X-ray should raise suspicion for PE.

Management:

Unfractionated Heparin: Metabolized by liver, used in renal insufficiency. Has short half-life. Given intravenously.

Low molecular weight Heparin(LMWH): cleared by kidney. Given subcutaneously.

Xa inhibitors: RivaroXaban.

Special scenario.

If the patient has a contrast allergy with renal failure. Avoid CT angiography. Do V/Q scanning.

-Unstable PE, Echocardiography shows right heart strain.

-If anticoagulants are contraindicated (recent brain bleeding), IVC can be placed.

TUMORS

Tumors of Head & Neck

HPV: Loves stratified squamous cells (oropharynx, true vocal cords, cervix, external anal canal. Produces E6, and E7 which inactivates P53, and RB respectively.

EBV: loves respiratory epithelium(Nasopharynx). Characterized by otitis media (Compression of Eustachian tube), hearing loss, nasal discharge, and obstruction.

Mediastinal tumors

Anterior mediastinum: 4Ts (thyroid, thymus, Teratoma, Terrible lymphoma).

Middle mediastinum: Metastases

Posterior mediastinum: Esophageal cancer, Neurofibroma.

How is it tested? A 45-year-old woman presents with ocular muscle weakness, particularly when looking at the ceiling for a short period. She also reports voice fatigue, with her speech becoming muffled after prolonged conversation.

LUNG AND PLEURAL TUMORS

Lung Cancers:

-#1 leading cause of cancer-related death, 2nd most common tumor (excluding skin cancers).

-A single large, irregular mass suggests primary lung cancer, while multiple masses are more likely metastatic disease.

-Stable masses on serial chest X-rays are typically benign and not concerning.

Genetic Associations:

-Adenocarcinoma → KRAS, ALK (Think: Adenocarcinoma Lung ‘Kancer’).

-Small cell lung cancer: TP53 (SBLA syndrome)

Screening & Risk Factors:

-High-risk patients: Age >50 with ≥20 pack-year smoking history.

-Screening: Annual low-dose chest CT.

Neuromuscular Associations:

-Lambert-Eaton Myasthenic Syndrome → Small cell lung cancer (proximal lower extremity weakness, ↓ reflexes).

-Myasthenia Gravis → Thymoma (distal upper extremity weakness, normal reflexes, affects ocular muscles).

Type	Location	Key Features	Markers/Histology
Small Cell Lung Cancer (SCLC)	Central	Aggressive, poor prognosis, paraneoplastic syndromes (SIADH, Cushing’s)	Chromogranin A (+), Synaptophysin (+), Neuron-Specific Enolase (+)
Adenocarcinoma	Peripheral	Most common in females, associated with clubbing (hypertrophic osteoarthropathy)	Mucin (+)
Squamous Cell Carcinoma	Central	Bronchial compression → recurrent pneumonia, hypercalcemia (PTHrP), Asbestos exposure: SCC > Mesothelioma	Keratin pearls, intercellular bridges
Carcinoid Tumor	Variable	Produces serotonin → flushing, diarrhea, wheezing (Carcinoid Syndrome)	Chromogranin A (+)
Pancoast Tumor (Superior Sulcus Tumor)	Apex	Compresses regional structures, causing unilateral symptoms: Shoulder pain, atrophy (brachial plexus); UE swelling (brachiocephalic vein); Horner’s syndrome (miosis, ptosis, anhidrosis); Hoarseness (recurrent laryngeal nerve); Hemidiaphragm paralysis (phrenic nerve)	N/A
SVC Syndrome	Mediastinum (due to tumor/thrombus)	Bilateral UE swelling (SVC), Neck swelling, JVD, ↑ Intracranial pressure → dizziness, aneurysm	N/A

How is tested? A 60-year-old nonsmoker female presents with weight loss and fatigue. CXR shows a single peripheral lung mass. What’s the Dx? A: Adenocarcinoma.

NOTE. Clubbing occurs due to the local release of PDGF and VEGF. It is NOT typically seen in COPD. When clubbing is present in a patient with COPD, it may suggest an underlying lung cancer.

Pleural tumors

Mesothelioma

-Associated with asbestos exposure (SCC of the lung is far more common in asbestos-exposed individuals).

– Tobacco smoking is NOT a risk factor for mesothelioma.

– Histology: Characterized by long microvilli and tonofilaments.

– Markers: Calretinin-positive, cytokeratin-positive.

How is it tested? A 65-year-old patient with a 10-year history of working in shipyards. What’s the most common cancer to develop? A: SCC of the lung (NOT mesothelioma)

Classic chest X-rays in Acute Emergencies

Tension Pneumothorax: A 25-year-old male involved in a motor vehicle accident presents with dyspnea and chest pain. His vital signs are as follows: he is hypotensive, tachycardiac, tachypneic low saturation. On examination, there are ↓ breath sounds on the left side with hyperresonance on percussion. A chest X-ray reveals hyperlucency on the left lung field with a mediastinal shift to the right, along with evidence of lung collapse. Management: needle decompression or chest tube.

Pleural effusion: A 30-year-old male is brought to the emergency department after sustaining a stab wound to the left side of the chest. He is complaining of severe chest pain and progressive shortness of breath. On examination, he is hypotensive, tachycardic, and tachypneic. Physical exam reveals decreased breath sounds on the left side with dullness to percussion. Laboratory investigations show a low hemoglobin level of 8 g/dL. A chest X-ray reveals a dense opacification of the left hemithorax with a blunted costophrenic angle.

Asthma exacerbation: A 22-year-old woman with a history of asthma presents to the emergency department with severe shortness of breath, wheezing, and chest tightness that started 2 hours ago after exposure to dust while cleaning. She reports increased use of her rescue inhaler with minimal relief. She denies fever, cough, or recent illness. On examination, she is tachypneic, and tachycardic, and has an oxygen saturation of 91%. She is using accessory muscles, and auscultation reveals bilateral wheezing with a prolonged expiratory phase (wheezes are absent is a severe exacerbation)CXR Findings: hyperinflation with flattened diaphragms due to air trapping.

Foreign body aspiration A 4-year-old boy is brought to the emergency department by his parents due to persistent cough, wheezing, and difficulty breathing for the past 6 hours. His symptoms began suddenly while playing with small toys, but no choking episode was witnessed. On examination, he is tachypneic, with mild respiratory distress. Auscultation reveals wheezing predominantly on the left side, and he was initially diagnosed with asthma exacerbation. He is prescribed an albuterol inhaler, but despite multiple doses, his wheezing and respiratory distress persist.

Due to lack of improvement, a repeat chest X-ray is performed, revealing hyperinflation of the left lung with a mediastinal shift to the right, raising concern for a foreign body aspiration causing partial bronchial obstruction.

NOTE. food particles do NOT show up in X ray but metal coins do.

Acute pulmonary embolism: A 28-year-old woman presents to the emergency department with sudden-onset pleuritic chest pain, dyspnea, and hemoptysis that began earlier in the day. She has a history of recent long-haul travel and is on oral contraceptive pills. On examination, she is tachycardic, tachypneic, and mildly hypoxic. Her blood pressure is 110/70 mmHg.

A chest X-ray is obtained and reveals Hampton’s hump, along with a small pleural effusion causing blunting of the right costophrenic angle, raising suspicion for pulmonary infarction due to acute pulmonary embolism. Sudden onset is an important clue for PE.

Flail chest and pulmonary contusion: A 35-year-old male presents after a motor vehicle collision with severe right-sided chest pain and worsening dyspnea. He is tachycardic, tachypneic, and has 94% SpO₂. Exam reveals right chest wall tenderness, crepitus, and decreased breath sounds. Chest X-ray shows multiple right-sided rib fractures with an underlying patchy alveolar infiltrate, consistent with pulmonary contusion. No pneumothorax or hemothorax is seen.

Acute pulmonary edema: A 65-year-old male with a history of hypertension and heart failure presents with sudden-onset dyspnea, orthopnea, and pink frothy sputum. He is hypertensive, tachypneic, and has bilateral crackles on lung auscultation. Chest X-ray shows an enlarged cardiac silhouette, perihilar opacities in a bat-wing pattern, Kerley A and B lines, and blunted costophrenic angles from bilateral pleural effusions.

Aortic dissection: A 60-year-old male with hypertension presents with sudden, severe chest pain radiating to the back. He is hypertensive, tachycardic, and has asymmetric pulses. Chest X-ray shows mediastinal widening, a prominent aortic knob, and convexity of the ascending aorta. CT angiography confirms a dilated ascending aorta with a dissection flap extending from the root to the descending aorta.

Type of atelectasis

Type	Cause	Example
Obstructive	Airway blockage	Tumor inside the bronchi
Compressive	External compression	Pleural effusion, pneumothorax
Contraction	Fibrosis causing lung retraction	Inflammation, TB fibrosis
Adhesive	Adhesive	Neonatal Respiratory Distress Syndrome (NRDS)

Patient Positioning and Clinical Indications

-Lying lateral (on the unhealthy side): Worsens oxygenation in pneumonia.

-Trendelenburg: Reduces air embolism risk.

-Supine (45° Reclined): Improves comfort & oxygenation in CHF/pulmonary edema, and reduces aspiration risk.

-Neck Flexed: Reduces aspiration risk.

-Prone: Enhances oxygenation in ARDS, and promotes posterior lung expansion.

NOTE. In a patient with left-sided pneumonia, pulmonary vasodilation occurs due to inflammation. Lying on the left side ↑blood flow to the affected lung due to gravity, worsening oxygenation. To improve oxygenation, the patient should lie on the healthy, unaffected side.

H. influenza (Typeable), S. pneumoniae, and Moraxella catarrhalis share common features:

-They cause otitis media, sinusitis, and acute exacerbations of COPD.

-Their capsule serves as a key virulence factor, aiding in immune evasion.

High Yield facts in children

-Croup: barking cough and stridor following an upper respiratory infection (URI). Caused by the Parainfluenza virus.

– Bronchiolitis: wheezing, cough, and respiratory distress after a URI. Most commonly caused by Respiratory Syncytial Virus (RSV) and is common in children up to 2 years. High-risk premature infants may receive Palivizumab, which targets the F (fusion) protein of RSV for prophylaxis.

– Diphtheria: sore throat, grayish pseudomembrane, and cervical lymphadenopathy.

Pleural effusions

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Pneumonia

– Typical Pneumonia: Lobar (Affects one lobe or one Lung) and Bronchopneumonia (affects area around bronchi, bronchioles)

– Atypical pneumonia: interstitial pneumonia (tissues between alveoli)

Most common organisms

Type	Common Organisms
Lobar Pneumonia	**Streptococcus pneumoniae (most common), Klebsiella pneumoniae**
Bronchopneumonia	**Staphylococcus aureus, Haemophilus influenzae**
Interstitial Pneumonia	Mycoplasma pneumoniae, Legionella pneumophila, viruses (e.g., Influenza, RSV, CMV)

– NOTE. Phases of lobar pneumonia: Congestion (bacterial proliferation, capillary dilation) → Red Hepatization (RBCs, neutrophils, fibrin; liver-like appearance) → Gray Hepatization (RBC breakdown, WBC & fibrin exudate) → Resolution (macrophages clear debris, lung recovers).

Strep pneumonia is the most common cause of community-acquired pneumonia even in patients with HIV (NOT PCP).

How is it tested? An HIV patient with CD4 of 140 developed fever, dyspnea, and chest pain for the last 2 days. CXR shows right lower lobe infiltrates. What’s the most likely organism? A: S.pneumonia (NOT PCP)

-Organisms such as Mycoplasma, Pneumocystis jirovecii (PCP), and fungi typically cause subacute symptoms. In contrast, acute infections, such as those caused by Streptococcus pneumoniae, present rapidly within 1–3 days with high fever and more severe symptoms.

-Some atypical organisms, such as Mycoplasma (which requires cholesterol for growth), lack a cell wall, making antibiotics that target the cell wall ineffective. Instead, prescribe Azithromycin– Mycoplasma is associated with cold agglutinin. Developing anemia after subacute pneumonia, think of Mycoplasma.

-Klebsiella pneumoniae is common in alcoholics, often affecting the upper lung zones and producing currant jelly sputum It is MacConkey agar positive, forming pink mucoid colonies.

– Neonatal pneumonia: Group B Strep (GBS), E. coli, Listeria.

–Post-viral pneumonia: S. aureus, S. pneumoniae, H. influenzae after influenza infection.

-Legionella pneumonia (requires Cysteine for growth): Initially presents with GI symptoms (e.g., diarrhea) followed by pulmonary symptoms. Associated with hyponatremia.

-Post-viral pneumonia (history of URI in elderly patient then pneumonia symptoms): S. aureus, S. pneumoniae, H. influenzae after influenza infection

How is it tested?

An 80-year-old man developed influenza symptoms. After a few days, he developed fever, chest pain, and crackles on the right lower lobe. What’s the most likely organism? A: staph aureus or strep. Pneumonia.
A neonate developed tachypnea, tachycardia, and fever. CXR shows diffuse bilateral infiltrates. Bronchial aspiration shows organisms that produce a green metallic sheen on EMB agar. What’s the organism? A: E.coli

High-yield pulmonary fungal infections

Fungus	Geographic Distribution / Risk Factors	Key Features
Histoplasma capsulatum	Ohio & Mississippi River valleys, bird/bat droppings	Granulomatous disease, intracellular yeast in macrophages
Blastomyces dermatitidis	Great Lakes	Broad-based budding yeast, lobar pneumonia, dermatological lesions (pustules, ulcers, verrucous lesions)
Coccidioides immitis	Southwestern U.S., desert soil, dust exposure (Desert Rheumatism)	Spherules with endospores, bone lesions, erythema nodosum.
Aspergillus spp.	Ubiquitous, affects immunocompromised, old TB cavities	Aspergilloma (fungus ball), Allergic bronchopulmonary aspergillosis (ABPA) in asthma, invasive aspergillosis in neutropenia
Pneumocystis jirovecii	HIV/AIDS (CD4 <200), immunosuppression	Diffuse interstitial pneumonia, silver stain positive, ground-glass opacities on CXR/CT
Cryptococcus neoformans	Pigeon droppings, immunocompromised (HIV, transplant)	Pulmonary nodules, meningitis, India ink positive

Hypersensitivity Pneumonitis (HP): A Type III/IV hypersensitivity reaction patient usually lives in a rural area and presents with recurrent episodes of dyspnea, cough, and low-grade fever, often resolving quickly with corticosteroids and removal of exposure. May initially improve with antibiotics, leading to misdiagnosis. Chronic exposure can lead to fibrosis and restrictive lung disease. Biopsy shows incomplete non-caseating granuloma formation.

How is it tested? A 35-year-old farmer presents to the clinic with recurring symptoms of dyspnea, cough and chest pain. prior episodes quickly resolved with Corticosteroids and antibiotics. CXR shows bilateral reticulonodular infiltrates. Biopsy shows granuloma. what’s the Dx? A: Hypersensitivity pneumonitis.

Granuloma formation: is driven by T-helper cells (IFN-γ) and macrophages (IL-12), leading to giant cell formation. IL-12 deficiency increases the risk of disseminated TB.

Pathogenesis

Early (Days): Neutrophils attack but fail to eliminate pathogens.
Macrophage Phase (Week 1): Macrophages engulf but cannot clear the infection.
Lymphocyte Phase (Weeks): Th1 cells (IFN-γ) activate macrophages, leading to granuloma formation.

Sarcoidosis

Middle-aged African American women, emphasizing the role of ethnicity. It typically presents with dyspnea, and CXR shows bilateral hilar lymphadenopathy. Hypercalcemia occurs due to ↑1α-hydroxylase activity in macrophages. Chronic disease can lead to fibrosis. Other associations include uveitis and erythema nodosum (Löfgren syndrome). Diagnosis is confirmed by biopsy showing non-caseating granulomas. Serum ACE and Vitamin D levels are not diagnostic. Glucocorticoids are the first-line treatment.

Tuberculosis

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Caseating granulomatous disease. Classic scenario is an immigrant from developing country, homeless or imprisoned patient who presents with fever, night sweats, hemoptysis, and weight loss.

-Primary TB typically affects the lower lung lobes, while secondary TB involves the upper lung lobes (as seen on radiographs).

–Interferon-gamma release assay (IGRA) is preferred over PPD skin testing in patients with prior BCG vaccination. PPD testing should be done before starting TNF-α inhibitors to prevent TB reactivation. False-negative

-PPD results may occur in HIV patients due to reduced T-helper cells. Cultures take 2–6 weeks, while sputum microscopy is faster but less sensitive.

-Cord factor forms a serpentine cord, acting as a virulence factor, while surface glycolipids inhibit phagocytosis.

How is it tested? A 50-year-old attended the clinic for a pre-employment evaluation. The patient is an immigrant and was administered BCG during childhood. PPD test is positive. CXR is clear. What’s the diagnosis? A: Latent Tb ( requires treatment)

Pneumoconioses develop after years of exposure; a few months of work is usually insufficient.

Type	Cause	Example	Findings	Complications
Obstructive	Airway blockage	Tumor inside the bronchi	Ferruginous bodies (golden-brown, iron-coated fibers in BAL)	Lung cancer (SCC > mesothelioma), pleural plaques, diaphragmatic plaques
Compressive	External compression	Pleural effusion, Pneumothorax	Eggshell calcification of hilar lymph nodes	↑ Risk of TB (disrupts phagolysosomal function)
Contraction	Fibrosis causing lung retraction	Inflammation, TB fibrosis	Small rounded opacities (dust within macrophages)	Fibrosis
Adhesive	Adhesive	Neonatal Respiratory Distress Syndrome (NRDS)	Non-caseating granulomas (similar to sarcoidosis)	Pulmonary fibrosis, systemic granulomatous disease

ARDS: due to acute injury (e.g. trauma, sepsis) it’s due to inflammation and increased vascular permeability

NRDS: due to surfactant deficiency in premature infants.

The hallmark of ARDS is a ↓ PaO₂/FiO₂ ratio (normal >300). For example, if PaO₂ is 50 in room air (21% O₂), then the PaO₂/FiO₂ ratio is: PaO₂/FiO₂ = 50 / 0.21 = 238. This indicates ARDS.

In ARDS management:–↑ PEEP (Positive End-Expiratory Pressure) to improve oxygenation.

-Use lower tidal volumes to reduce ventilator-associated lung injury

Obstructive sleep apnea vs obesity hypoventilation syndrome.

Feature	Obstructive Sleep Apnea (OSA)	Obesity Hypoventilation Syndrome (OHS)
PaO₂ (Daytime)	N	↓
PaCO₂ (Daytime)	N	↑

OSA in children can be associated with tonsillar and adenoid hypertrophy. It may present with symptoms similar to ADHD and depression.

Treatments

Antihistamines are divided into first and second generations.

– First-generation (Diphenhydramine, Chlorpheniramine, Doxylamine) are sedating and have antimuscarinic (urinary retention) and anti-α adrenergic (orthostatic hypotension) effects, posing a higher risk in the elderly. Doxylamine + Pyridoxine is used for nausea and vomiting in pregnancy. They should not be combined with other sedating agents like benzodiazepines.

-Second-generation (Loratadine, Cetirizine) is less sedating due to poor CNS penetration.

Pseudoephedrine and Phenylephrine, α-adrenergic agonists, treat nasal congestion, but prolonged use (>7 days) can cause rhinitis medicamentosa due to neurotransmitter depletion and α-receptor internalization.

Asthma Medications target inflammation and ↑parasympathetic tone.

–β2-agonists relax smooth muscle but can cause tremors and hypokalemia in overdose. Albuterol (short-acting) is used for intermittent symptoms, while Salmeterol and Formoterol are used for maintenance therapy.

How is it tested? A patient with severe asthma requires multiple doses of albuterol. What’s the most probable side effect? A: Tremors

Inhaled glucocorticoids (Fluticasone, Budesonide) inhibit NF-κB, reducing inflammatory cytokines. A major side effect is oral thrush, which can be prevented by using a spacer.

Muscarinic antagonists relax smooth muscle and ↓ mucus production; Ipratropium is short-acting, while Tiotropium is long-acting.

How is it tested? A COPD patient was administered a medication that decreased salivation and mucous production. What’s the mechanism of action? A: Muscarinic antagonist.

Anti-IgE monoclonal antibody (Omalizumab) binds to serum IgE, preventing its interaction with FcεRI. It is used for drug-resistant asthma.

Leukotriene inhibitors include Zileuton (5-LOX inhibitor) and Montelukast (leukotriene receptor blocker).

Theophylline, a phosphodiesterase inhibitor, ↑cAMP but has a narrow therapeutic index. CYP450 inhibitors (cimetidine, fluconazole, clarithromycin, grapefruits) can raise its serum levels, leading to palpitations, cardiotoxicity, and seizures. It also blocks adenosine action.

How is it tested? A patient with advanced COPD taking Theophylline. He is recently treated for fungal infection. He started developing tremors and palpitations. What’s the mechanism of action? inhibits the P450 system.

PDE-4 inhibitor (Roflumilast) ↑cAMP and is used in COPD.

Cromolyn is a mast cell stabilizer.

Anti-IL5 monoclonal antibodies prevent eosinophil differentiation, reducing eosinophilic inflammation.

SIDE NOTE. Key cytokine functions: IL-4 → IgE production, IL-5 → IgA and eosinophil production.

COPD: interventions have been shown to ↓ mortality in COPD

smoking cessation (MOST EFFECTIVE)
long term oxygen therapy ( PaO₂ ≤ 55 mmHg or SaO₂ ≤ 88%).

NOTE. A saturation above 88% is unlikely to be beneficial over the long term.

-bronchodilators and corticosteroids improve symptoms and reduce exacerbations but do NOT significantly reduce mortality

Pulmonary hypertension medications

Endothelin receptor blockers (e.g., Bosentan) reduce vasoconstriction by blocking endothelin-1 receptors.

PDE-5 inhibitors (e.g. Sildenafil) ↑cGMP, enhancing NO-mediated vasodilation. They should not be used with nitrates due to the risk of severe hypotension.

Prostacyclin (PGI₂) analogs (e.g., Epoprostenol) act as vasodilators and platelet inhibitors. It may cause flushing and jaw pain.

NOTE. Endothelin and angiotensin are potent vasoconstrictors.

How is it tested? A 20-year-old woman with PAH is prescribed a medication that increases pulmonary blood flow by preventing its degradation to inactive substances. What’s this med? A: Sildenafil

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USMLE Step 1 High‐Yield Respiratory/Pulmonology Topics

Respiratory / Pulmonology

High Yield USMLE Step 1 Notes

Table of Contents

Embryology

Anatomy & Histology

Physiology

Physiological changes during exercise;

Infections / Inflammatory Conditions

Comparison of physical exam finding in common pulmonary conditions

Tuberculosis Pathogenesis

Obstructive / Restrictive Diseases

Flow volume loops of Obstructive VS restrictive lung diseases

Respiratory Neoplasms

Lung Cancer Types:

Respiratory Pathologies (Other)

Pharmacology

🏁 Final Thoughts

Disclaimer

Narrative Format

High-Yield Respiratory / Pulmonology Topics

Table of Contents

Embryology

Pulmonary hypoplasia

Anatomy & Histology

Type of Epithelium

IMPORTANT LEVELS

Intercostal nerve block

Physiology

Fibrosis Vs Emphysema

High Yield concepts

Acid-Base disorders

Oxygen Hemoglobin Dissociation Curve

SIDE NOTES

Pathology

Flow-volume Loop

Obstructive lung disease Vs restrictive lung disease

Cystic Fibrosis vs. Kartagener Syndrome

DVT/PE

TUMORS

Tumors of Head & Neck

Mediastinal tumors

LUNG AND PLEURAL TUMORS

Pleural tumors

Classic chest X-rays in Acute Emergencies

Type of atelectasis

Patient Positioning and Clinical Indications

High Yield facts in children

Pleural effusions

Pneumonia

Most common organisms

High-yield pulmonary fungal infections

Pathogenesis

Sarcoidosis

Tuberculosis

Treatments

Pulmonary hypertension medications

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