Respiratory Pathology — MCQs
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What is a characteristic feature of shock lung?
Which of the following statements is true about Non-specific interstitial pneumonia?
A 72-year-old woman presents with a 3-month history of difficulty with vision in her right eye and pain in the right upper chest. Physical examination reveals unilateral enophthalmos, miosis, anhidrosis, and ptosis on the right side of her face. A chest radiograph shows right upper lobe opacification and bony destruction of the right first rib. Which of the following conditions is most likely present?
Which of the following is NOT typically seen in ARDS?
Which of the following is NOT a stage of pneumonia?
Kartagener's syndrome is associated with an increased risk of which of the following conditions?
A specimen from a lung biopsy reveals occasional plexiform lesions within pulmonary arterioles. Which of the following conditions is most characteristic of this finding?
What is the most common type of emphysema?
What is the term for mucus plugs containing epithelial cell aggregations arranged as whorls of shed epithelium, observed in bronchial asthma?
Which of the following is true about bronchial carcinoids?
Respiratory Pathology Indian Medical PG Practice Questions and MCQs
Question 1: What is a characteristic feature of shock lung?
- A. Diffuse alveolar damage (Correct Answer)
- B. Usual interstitial pneumonitis
- C. Organizing pneumonia
- D. Bronchiolitis
Explanation: **Explanation:** **Shock lung** is the clinical-pathological term for **Acute Respiratory Distress Syndrome (ARDS)**. The hallmark pathological finding of ARDS/shock lung is **Diffuse Alveolar Damage (DAD)** [1]. **1. Why Diffuse Alveolar Damage (DAD) is correct:** DAD is the common pathway for various insults (shock, sepsis, trauma, or pneumonia). It occurs in two main phases: * **Exudative Phase:** Characterized by capillary congestion, interstitial edema, and the formation of **hyaline membranes** (composed of fibrin and necrotic cell debris) lining the alveolar walls [1]. * **Organizing/Proliferative Phase:** Characterized by Type II pneumocyte proliferation and fibroblast infiltration [1]. **2. Why the other options are incorrect:** * **Usual Interstitial Pneumonitis (UIP):** This is the histological pattern of Idiopathic Pulmonary Fibrosis (IPF). It is a chronic, progressive fibrotic condition characterized by "spatial and temporal heterogeneity" (old and new fibrosis), not acute shock. * **Organizing Pneumonia:** Formerly known as BOOP, this involves polypoid plugs of loose connective tissue (Masson bodies) within alveolar ducts and alveoli [2]. * **Bronchiolitis:** This refers to inflammation of the small airways, often viral (RSV) or related to smoking, rather than diffuse alveolar injury. **High-Yield Clinical Pearls for NEET-PG:** * **Hyaline membranes** are the most characteristic microscopic feature of the acute phase of DAD [1]. * **Pathogenesis:** The primary injury is to the **alveolar capillary endothelium** and **Type I pneumocytes** [1]. * **Neutrophils** play a key role in the pathogenesis by releasing ROS and proteases. * **Radiology:** Shows bilateral "white-out" or diffuse opacities on chest X-ray [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 679-681. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 693-695.
Question 2: Which of the following statements is true about Non-specific interstitial pneumonia?
- A. Early appearance of honeycombing on CT
- B. Males are affected more commonly than females
- C. Common in the elderly age group
- D. Associated with a good prognosis (Correct Answer)
Explanation: **Explanation:** **Non-specific Interstitial Pneumonia (NSIP)** is a distinct pattern of chronic interstitial lung disease that is crucial to differentiate from Usual Interstitial Pneumonia (UIP/Idiopathic Pulmonary Fibrosis). **Why Option D is Correct:** NSIP is characterized by a much **better prognosis** compared to UIP [1]. Patients typically respond well to oral corticosteroids, and the 5-year survival rate is significantly higher (approx. 80-100% for the cellular variant) than that of UIP (approx. 30-50%) [1]. **Analysis of Incorrect Options:** * **Option A:** Honeycombing is **rare and occurs very late** in NSIP [1]. On HRCT, the hallmark finding is **Ground Glass Opacities (GGO)**, usually in a symmetrical, subpleural distribution with "subpleural sparing." Honeycombing is the classic early/diagnostic feature of UIP. * **Option B:** Unlike many other interstitial diseases, NSIP shows a **female predilection**, particularly in non-smokers [1]. * **Option C:** NSIP typically affects a **younger age group** (40–50 years) compared to UIP, which is predominantly a disease of the elderly (usually >60 years). **High-Yield Clinical Pearls for NEET-PG:** 1. **Histological Variants:** NSIP is divided into **Cellular** (better prognosis, inflammatory infiltrate) and **Fibrotic** (worse prognosis, dense collagen) patterns [1]. 2. **Key Association:** NSIP is the most common pulmonary manifestation of **Systemic Sclerosis (Scleroderma)** and other Connective Tissue Diseases (CTDs). 3. **Temporal Homogeneity:** Unlike UIP, which shows "temporal heterogeneity" (old and new lesions together), NSIP lesions are **temporally homogeneous** (all lesions appear to be of the same age) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 693-695.
Question 3: A 72-year-old woman presents with a 3-month history of difficulty with vision in her right eye and pain in the right upper chest. Physical examination reveals unilateral enophthalmos, miosis, anhidrosis, and ptosis on the right side of her face. A chest radiograph shows right upper lobe opacification and bony destruction of the right first rib. Which of the following conditions is most likely present?
- A. Bronchopneumonia
- B. Bronchiectasis
- C. Bronchogenic carcinoma (Correct Answer)
- D. Sarcoidosis
Explanation: ### Explanation **Correct Answer: C. Bronchogenic carcinoma** The clinical presentation describes a classic case of a **Pancoast tumor** (Superior Sulcus Tumor), which is most commonly a **Bronchogenic carcinoma** (typically Squamous cell carcinoma or Adenocarcinoma). 1. **The Underlying Concept:** A tumor located at the extreme apex of the lung can locally invade the **cervical sympathetic chain** and the **stellate ganglion** [1]. This leads to **Horner Syndrome**, characterized by the clinical triad of **ptosis** (drooping eyelid), **miosis** (constricted pupil), and **anhidrosis** (lack of sweating), along with **enophthalmos** [1]. The patient’s chest pain and bony destruction of the first rib indicate local invasion of the brachial plexus and thoracic outlet, further confirming a malignant process [1],[2]. **Why incorrect options are wrong:** * **A. Bronchopneumonia:** This is an acute infectious process presenting with fever, productive cough, and consolidation. It does not cause bony destruction or Horner syndrome. * **B. Bronchiectasis:** This involves permanent dilation of bronchi due to chronic infection. It presents with copious foul-smelling sputum and hemoptysis, not apical invasive masses [3]. * **D. Sarcoidosis:** While it can involve the lungs, it typically presents with bilateral hilar lymphadenopathy and non-caseating granulomas. It is not locally invasive enough to destroy ribs or cause Horner syndrome. **High-Yield Clinical Pearls for NEET-PG:** * **Pancoast Syndrome:** Horner syndrome + Shoulder/Arm pain + Wasting of hand muscles (due to C8-T2 nerve root involvement) [1]. * **Most common histology:** Squamous cell carcinoma was historically most common, but Adenocarcinoma is now frequently cited due to its peripheral location. * **Radiology:** Look for "apical cap" or opacification with associated rib erosion. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 334-335. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, p. 725. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 724-725.
Question 4: Which of the following is NOT typically seen in ARDS?
- A. Dilated bronchioles (Correct Answer)
- B. Edema
- C. Fibrosis
- D. Alveolar damage
Explanation: **Explanation:** Acute Respiratory Distress Syndrome (ARDS) is a clinical syndrome characterized by severe hypoxemia and bilateral pulmonary infiltrates, resulting from **Diffuse Alveolar Damage (DAD)** [2]. **Why "Dilated Bronchioles" is the correct answer:** Dilated bronchioles (bronchiectasis) are a feature of chronic, obstructive, or fibrotic lung diseases (like Cystic Fibrosis or late-stage IPFE), but they are **not** a characteristic feature of ARDS [1]. ARDS primarily affects the alveolar-capillary unit, leading to alveolar collapse (atelectasis) rather than airway dilation [3]. **Analysis of other options:** * **Alveolar Damage:** This is the pathological hallmark of ARDS. It involves injury to pneumocytes and endothelial cells, leading to the formation of characteristic **hyaline membranes** [1]. * **Edema:** The initial "exudative phase" of ARDS is defined by increased capillary permeability, leading to protein-rich fluid leaking into the alveolar spaces (non-cardiogenic pulmonary edema) [2]. * **Fibrosis:** In the "organizing/proliferative phase," there is a proliferation of Type II pneumocytes and fibroblasts. If the insult is severe or prolonged, it progresses to interstitial fibrosis [1]. **NEET-PG High-Yield Pearls:** * **Pathological Hallmark:** Diffuse Alveolar Damage (DAD) with Hyaline Membranes (composed of fibrin and cell debris) [1]. * **Berlin Criteria:** Acute onset (within 1 week), bilateral opacities on imaging, and $PaO_2/FiO_2$ ratio < 300 mmHg (with PEEP $\geq$ 5 cm $H_2O$) [2]. * **Key Cytokine:** IL-8 is a potent neutrophil chemoattractant central to the pathogenesis. * **Morphological Phases:** 1. Exudative (0-7 days), 2. Proliferative/Organizing (1-3 weeks), 3. Fibrotic (>3 weeks) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 679-681. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, p. 679. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, p. 681.
Question 5: Which of the following is NOT a stage of pneumonia?
- A. Stage of Exudation
- B. Stage of Red Hepatization
- C. Stage of Cavitation (Correct Answer)
- D. Stage of Resolution
Explanation: ### Explanation The question asks to identify which option is **not** a classic stage of lobar pneumonia. [1] **Why "Stage of Cavitation" is the Correct Answer:** Lobar pneumonia, typically caused by *Streptococcus pneumoniae*, follows a predictable sequence of pathological stages (Congestion, Red Hepatization, Grey Hepatization, and Resolution). [1], [3] **Cavitation** is not a standard stage; rather, it is a **complication** of pneumonia. Cavitation occurs when there is significant tissue necrosis (abscess formation), commonly associated with specific virulent organisms like *Staphylococcus aureus* or *Klebsiella pneumoniae*, but it is not part of the typical evolution of lobar pneumonia. [2] **Analysis of Incorrect Options:** * **Stage of Exudation (Congestion):** This is the initial stage (first 24 hours). The lung is heavy, boggy, and red. Histology shows vascular engorgement, intra-alveolar fluid with few neutrophils, and numerous bacteria. [1], [3] * **Stage of Red Hepatization:** Occurs within 2–4 days. The lung becomes liver-like in consistency. The alveoli are packed with exudate containing erythrocytes (RBCs), neutrophils, and fibrin. [1], [3] * **Stage of Resolution:** The final stage (if no complications occur). The accumulated exudate undergoes enzymatic digestion by macrophages, which is then either coughed up or resorbed, restoring normal lung architecture. [1], [4] **NEET-PG High-Yield Pearls:** 1. **Grey Hepatization:** Occurs between Red Hepatization and Resolution (Days 4–8). RBCs disintegrate, and the lung appears grayish-brown due to persistent fibrinopurulent exudate. [1], [3] 2. **Most Common Cause:** *Streptococcus pneumoniae* (Pneumococcus) is the most common cause of community-acquired lobar pneumonia. [2] 3. **Hepatization:** This term refers to the lung parenchyma losing its air-filled sponginess and becoming solid/firm, resembling liver tissue. [1] 4. **Complications:** If resolution fails, complications include **Organization** (fibrosis), **Abscess** (cavitation), **Empyema**, or **Bacteremic dissemination**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 711-712. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, p. 715. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 317-318. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 193-194.
Question 6: Kartagener's syndrome is associated with an increased risk of which of the following conditions?
- A. Bronchitis
- B. Bronchiolitis
- C. Bronchiectasis (Correct Answer)
- D. Tracheitis
Explanation: **Explanation:** **Kartagener’s Syndrome** is a clinical triad consisting of **Situs Inversus, Chronic Sinusitis, and Bronchiectasis**. It is a subset of **Primary Ciliary Dyskinesia (PCD)**, an autosomal recessive disorder characterized by structural abnormalities in the cilia, most commonly a defect in the **outer and/or inner dynein arms**. 1. **Why Bronchiectasis is correct:** Cilia are essential for the "mucociliary escalator," which clears inhaled particles and pathogens from the respiratory tract. In Kartagener’s syndrome, the cilia are immotile or dyskinetic, leading to chronic mucus stasis and recurrent infections [2]. This persistent inflammation causes permanent, abnormal dilation of the bronchi and destruction of the muscular and elastic components of the bronchial walls, which is the definition of **Bronchiectasis** [1], [2]. 2. **Why other options are incorrect:** * **Bronchitis and Bronchiolitis:** While these involve inflammation of the airways, they are typically acute or reversible conditions. Kartagener’s leads to the *permanent* structural damage seen in bronchiectasis. * **Tracheitis:** This is an acute bacterial infection of the trachea (often by *S. aureus*). While patients with PCD are prone to infections, the hallmark pathological sequela of the syndrome is lower airway destruction (bronchiectasis), not isolated tracheitis. **High-Yield Clinical Pearls for NEET-PG:** * **Genetic Defect:** Mutations in *DNAH5* and *DNAI1* genes (coding for dynein). * **Infertility:** Males are infertile due to **immotile spermatozoa** (the flagella share the same axonemal structure as cilia). Females may have reduced fertility due to impaired ciliary action in the fallopian tubes. * **Diagnosis:** Screened via low nasal Nitric Oxide (nNO) levels; confirmed by high-speed digital videomicroscopy or electron microscopy showing absent dynein arms. * **Radiology:** Look for "Tram-track" opacities on CXR/CT (indicative of bronchiectasis) and dextrocardia [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 690-691. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 321-322.
Question 7: A specimen from a lung biopsy reveals occasional plexiform lesions within pulmonary arterioles. Which of the following conditions is most characteristic of this finding?
- A. Churg-Strauss syndrome
- B. Adult respiratory distress syndrome
- C. Wegener's granulomatosis
- D. Pulmonary hypertension (Correct Answer)
Explanation: **Explanation:** The presence of **plexiform lesions** is a pathognomonic histological hallmark of **Primary Pulmonary Hypertension (PPH)** or severe, long-standing secondary pulmonary arterial hypertension [1]. 1. **Why Pulmonary Hypertension is correct:** Plexiform lesions are complex, tuft-like proliferations of endothelial cells, fibroblasts, and smooth muscle cells that form small capillary-like channels within the lumen of dilated, thin-walled small pulmonary arterioles [1]. They typically occur in **Grade IV** of the Heath-Edwards classification of pulmonary hypertension, representing advanced vascular remodeling due to chronic high pressure and shear stress. 2. **Why other options are incorrect:** * **Churg-Strauss Syndrome (EGPA):** Characterized by eosinophil-rich granulomatous inflammation, necrotizing vasculitis, and a strong clinical association with asthma and peripheral eosinophilia. * **Adult Respiratory Distress Syndrome (ARDS):** The hallmark is **Diffuse Alveolar Damage (DAD)** with the formation of waxy hyaline membranes lining the alveolar walls, not vascular remodeling. * **Wegener’s Granulomatosis (GPA):** Characterized by a "geographic" pattern of necrosis, granulomatous inflammation of the respiratory tract, and necrotizing vasculitis. It is strongly associated with **c-ANCA (PR3-ANCA)**. **High-Yield Clinical Pearls for NEET-PG:** * **Heath-Edwards Grading:** Grade I (Medial hypertrophy), Grade II (Intimal proliferation), Grade III (Intimal fibrosis), **Grade IV (Plexiform lesions)**. * **Genetic Link:** Mutations in the **BMPR2** gene (Bone Morphogenetic Protein Receptor type 2) are the most common cause of heritable pulmonary arterial hypertension [2]. * **Clinical Presentation:** Look for a young female with progressive dyspnea, a loud P2 (second heart sound), and right ventricular hypertrophy (cor pulmonale). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, p. 707. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 324-325.
Question 8: What is the most common type of emphysema?
- A. Centriacinar (Correct Answer)
- B. Panacinar
- C. Paraseptal
- D. Irregular
Explanation: **Explanation:** **1. Why Centriacinar is correct:** Centriacinar (centrilobular) emphysema is the **most common clinical type**, accounting for more than 95% of cases [1]. It is characterized by involvement of the central or proximal parts of the acini (respiratory bronchioles), while distal alveoli are spared [2]. This pattern is classically associated with **heavy cigarette smoking** and is most severe in the **upper lobes** of the lungs [1]. **2. Analysis of Incorrect Options:** * **Panacinar (Panlobular):** In this type, the acini are uniformly enlarged from the level of the respiratory bronchiole to the terminal blind alveoli [2]. It is characteristically associated with **$\alpha_1$-antitrypsin deficiency** and typically affects the **lower zones** of the lungs [3]. * **Paraseptal (Distal Acinar):** This involves the distal part of the acinus. It is often found near the pleura and along connective tissue septa [2]. While it usually doesn't cause significant airway obstruction, it is a common cause of **spontaneous pneumothorax** in young adults due to the rupture of subpleural blebs [2]. * **Irregular:** This is associated with scarring (healed inflammatory diseases). While it is technically the most common type found at autopsy (incidental finding), it is usually asymptomatic and clinically insignificant compared to centriacinar emphysema [2]. **3. NEET-PG High-Yield Pearls:** * **Definition:** Emphysema is defined morphologically as the irreversible enlargement of airspaces distal to the terminal bronchioles, accompanied by the destruction of their walls without obvious fibrosis [4]. * **Protease-Antiprotease Hypothesis:** The primary mechanism is an imbalance between elastase (from neutrophils/macrophages) and antielastases (like $\alpha_1$-AT) [3]. * **Pink Puffers:** Patients with predominant emphysema are often thin, barrel-chested, and dyspneic with near-normal blood gas levels until late in the disease. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 684-685. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, p. 683. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 683-684. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 326-327.
Question 9: What is the term for mucus plugs containing epithelial cell aggregations arranged as whorls of shed epithelium, observed in bronchial asthma?
- A. Charcot-Leyden crystals
- B. Curshmann spirals (Correct Answer)
- C. Creola bodies
- D. None of the above
Explanation: ### Explanation **Correct Answer: B. Curschmann spirals** **1. Why Curschmann spirals is correct:** In Bronchial Asthma, chronic inflammation leads to the hypersecretion of thick, tenacious mucus. **Curschmann spirals** are microscopic findings in the sputum or lavage of these patients. They consist of **coiled, spiral-shaped mucus plugs** that contain shed epithelial cells [1]. They represent a cast of the small distal airways (bronchioles) where the mucus has become inspissated and twisted. **2. Why other options are incorrect:** * **A. Charcot-Leyden crystals:** These are eosinophil-derived structures. They are composed of **galectin-10** (an eosinophil lysophospholipase binding protein) and appear as needle-like, rhomboid crystals. While found in asthma, they represent eosinophil breakdown rather than epithelial whorls. * **C. Creola bodies:** These are **compact clusters or "balls" of desquamated columnar epithelial cells**. While they are also found in the sputum of asthmatics, the question specifically describes "whorls" and "mucus plugs," which is the classic definition of Curschmann spirals. **3. NEET-PG High-Yield Pearls:** * **Triad of Sputum Findings in Asthma:** Curschmann spirals (mucus), Charcot-Leyden crystals (eosinophil protein), and Creola bodies (epithelial clusters). * **Airway Remodeling:** Key features include thickening of the basement membrane (Type I and III collagen), hypertrophy of bronchial smooth muscle, and goblet cell hyperplasia. * **Immunology:** Asthma is a **Type I Hypersensitivity** reaction mediated by **Th2 cells**, which secrete IL-4 (stimulates IgE), IL-5 (activates eosinophils), and IL-13 (stimulates mucus) [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 328-329.
Question 10: Which of the following is true about bronchial carcinoids?
- A. Highly radiosensitive
- B. Metastasis is common
- C. Carcinoid syndrome does not manifest (Correct Answer)
- D. Commonly arise from terminal bronchioles
Explanation: **Explanation:** **Bronchial Carcinoids** are neuroendocrine tumors arising from **Kulchitsky cells** (enterochromaffin cells) of the bronchial mucosa. **Why Option C is Correct:** While bronchial carcinoids are neuroendocrine tumors, **carcinoid syndrome is extremely rare** (occurring in <1% of cases). For carcinoid syndrome to manifest, vasoactive substances like serotonin must reach the systemic circulation. In bronchial carcinoids, these substances are usually inactivated by the lungs or the tumor burden is insufficient to produce systemic symptoms. This is a classic "distractor" because students often associate all carcinoids with the syndrome. **Why Other Options are Incorrect:** * **Option A:** Bronchial carcinoids are generally **radioresistant**. Surgical resection is the primary treatment of choice. * **Option B:** Most bronchial carcinoids (approx. 90%) are **Typical Carcinoids**, which are low-grade, slow-growing, and have a low metastatic potential (<15%) [1]. Atypical carcinoids have a higher rate but are less common. * **Option D:** They typically arise from **major/central bronchi** (central carcinoids), often presenting as polypoid, finger-like masses projecting into the lumen, leading to obstructive pneumonia or hemoptysis [1]. **High-Yield Pearls for NEET-PG:** * **Morphology:** Characterized by a "salt and pepper" chromatin pattern and organoid/nesting growth [1]. * **Markers:** Positive for **Chromogranin, Synaptophysin**, and CD56. * **Typical vs. Atypical:** Typical carcinoids have <2 mitoses/10 HPF and no necrosis; Atypical have 2-10 mitoses/10 HPF and focal necrosis [1]. * **Clinical Presentation:** Often presents with persistent cough, hemoptysis, or recurrent localized pneumonia. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 725-727.
Practice by Chapter
Congenital Anomalies
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Atelectasis and Acute Lung Injury
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Obstructive Pulmonary Diseases
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Restrictive Pulmonary Diseases
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Lung Tumors
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Pleural Diseases
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Interstitial Lung Diseases
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Occupational Lung Diseases
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