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Pulmonology Exam > Pathology of Lung Neoplasms and Infections > Flashcards

Pathology of Lung Neoplasms and Infections Flashcards

1
Q

causes of pneumonia

A
  1. impaired local defense mechanisms:
    -suppression of cough reflex
    -dysfunction of mucociliary apparatus
    -accumulation of secretions
    -interference with phagocytic alveolar macrophages
    -pulmonary congestion, edema
  2. immunodeficiency:
    -chronic diseases, immunologic deficiencies
    -immunosuppressive agents
    -leukopenia
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2
Q

pneumonia - clinical features

A

*fever, chills
*productive cough
*tachypnea, pleuritic chest pain
*decreased breath sounds
*dullness to percussion

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3
Q

diagnosis of pneumonia

A

*labs:
-CBC with elevated WBC
-sputum gram stain
-cultures (sputum, tissue, blood)
*CXR:
-lobar pneumonia
-bronchopneumonia
-interstitial pneumonia

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4
Q

lobar bacterial pneumonia

A

*consolidation (solid, airless) of ENTIRE LOBE
*alveoli filled with neutrophils; congested septa
*most common pathogen = Strep pneumo (gram positive diplococci)

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5
Q

bronchopneumonia

A

*PATCHY consolidation around bronchioles
*often multifocal and bilateral
*most common pathogen = Staph aureus (gram positive cocci)

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6
Q

lobar pneumonia vs. bronchopneumonia

A

*lobar pneumonia (left) most commonly strep pneumo
*bronchopneumonia (right) most commonly staph aureus

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7
Q

viral pneumonia - overview

A

*nearly all also cause upper-respiratory tract infections
*risk factors: extremes of age, malnutrition, debilitating illness
*organisms: INFLUENZA (types A and B), COVID19, RSV, adenovirus, etc

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8
Q

viral pneumonia - morphology

A

*congested lung w/ lymphocytic and monocytic reaction
-may be patchy or involve whole lobes, bilaterally or unilaterally
*severe infections lead to diffuse alveolar damage with hyaline membranes (ARDS)

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9
Q

viral pneumonia - pathogenesis

A

*viruses infect and damage respiratory epithelium; impaired local defenses predisposes to secondary bacterial infections

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10
Q

tuberculosis - primary infection

A

*previously un-sensitized
*clinical: asymptomatic in 95% of patients
*pathology: GHON COMPLEX on CXR
-focal caseation in parenchyma + hilar nodes
-undergoes fibrosis/calcification for imaging
*leads to PPD+

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11
Q

tuberculosis - secondary infection

A

*previously sensitized individuals
*YEARS after initial infection, reactivation of latent infection (or reinfection in the face of waning host immunity)
*clinical: fever, night sweats, cough, hemoptysis
*APICES OF LUNG are infected, causing poor lymphatic drainage and high O2 tenssion

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12
Q

tuberculosis - secondary infection PATHOLOGY

A

*cavitary lesion with CASEATING NECROSIS (caseous necrotizing granulomas)
*diagnosis: acid-fast positive bacilli

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13
Q

tuberculosis - progressive infection

A

*blood-borne spread (subsequent to primary or secondary infections)
*more common in immunosuppressed patients
*pathology: MILIARY (disseminated granulomas; spleen, liver, other organs)
*diagnosis: AFB+ bacilli, NUMEROUS

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14
Q

spectrum of tuberculosis pathologies

A
  1. primary: Ghon complex (lower lobe + hilar nodes)
  2. secondary: granuloma with caseation
  3. progressive: miliary = disseminated granulomas
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15
Q

spectrum of granulomas

A
  1. non-necrotizing:
    -think of sarcoid, fungi, foreign bodies, or autoimmune
  2. caseous, necrotizing:
    -think of TB
  3. suppurative, necrotizing:
    -think of bacteria, fungi, or foreign bodies
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16
Q

non-necrotizing granulomas

A

*think of sarcoid, fungi, foreign bodies, or autoimmune conditions

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17
Q

caseous, necrotizing granulomas

A

*think of TB

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18
Q

suppurative, necrotizing granulomas

A

*think of bacteria, fungi, or foreign bodies
*suppurative means neutrophils/bacteria

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19
Q

pulmonary abscess - overview

A

*local suppurative process, causing necrosis of lung tissue

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20
Q

pulmonary abscess - causes

A

*aspiration
*antecedent lung infection
*septic embolism
*secondary infection from obstructing neoplasm
*traumatic penetrations
*hematogenous seeding by pyogenic organisms

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21
Q

pulmonary abscess - clinical features

A

*cough with copious amounts of foul-smelling purulent or sanguineous sputum
*fever, chest pain, and weight loss are common
*diagnosis confirmed radiographically

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22
Q

pulmonary abscess - morphology

A

*suppurative parenchymal destruction with cavitation

23
Q

opportunistic pulmonary infections

A

*serious infections in immunocompromised individuals
*common organisms include:
-CMV
-pneumocystis jiroveci
-cryptococcus neoformans
-aspergillus

24
Q

pathology of opportunistic pulmonary infections: CYTOMEGALOVIRUS (CMV)

A

*huge cells with intranuclear inclusions surrounded by halo

25
Q

pathology of opportunistic pulmonary infections: PNEUMOCYSTIS JIROVECI

A

*intra-alveolar, foamy exudate
*silver+ cup-shaped cysts

26
Q

pathology of opportunistic pulmonary infections: CRYPTOCOCCUS NEOFORMANS

A

*granulomas with PAS+ encapsulated yeasts

27
Q

pathology of opportunistic pulmonary infections: ASPERGILLUS

A

*angio-invasive silver+ molds causing hemorrhage, necrosis

28
Q

hypertrophic pulmonary osteoarthropathy (HPO)

A

*aka digital clubbing (clubbing of the fingers)
*painful periosteal elevation at several bony and joint sites, especially the fingers
*elevation of the nail bed to form a pronounced curvature is characteristic
*associated with some pulmonary carcinomas, especially adenocarcinomas

29
Q

lung carcinoma - overview & epidemiology

A

*malignant neoplasm of pulmonary epithelial cells
*most frequently diagnosed major cancer and most common cause of cancer mortality worldwide
*incidence gradually decreasing (possibly due to changes in smoking habits?)
*peak incidence in adults 50+ in age
*prognosis remains dismal

30
Q

major causes of cavitary lesions in the lung

A
  1. pulmonary tuberculosis (most common)
  2. malignancy, especially squamous cell carcinoma
  3. lung abscess
31
Q

major histologic types of lung carcinoma

A
  1. small cell carcinoma
  2. non-small cell carcinoma:
    a. adenocarcinoma
    b. squamous cell carcinoma
    c. large cell carcinoma
32
Q

lung carcinoma - pathogenesis

A

*stepwise accumulation of carcinogen-induced driver mutation:
-“Field Effect” = genetic alterations seen in benign epithelium
-precursor lesions = preinvasive, antedate carcinoma:
~asymptomatic and undetectable on radiographs
~atypical cells identified in sputum, cytologic smears, tissue biopsies
~changes may last for years

33
Q

squamous cell carcinoma - overview

A

*malignant neoplasms of bronchial epithelium with SQUAMOUS CELL DIFFERENTIATION
*most common tumor in male smokers
*arise CENTRALLY in major bronchi:
-segmental/subsegmental bronchi
-become symptomatic with bronchial obstruction
-eventually spread to hilar nodes

34
Q

squamous cell carcinoma - pathogenesis

A

*highly associated with exposure to tobacco smoke
*diverse genetic aberrations:
-TP53 mutation
-CDKN2A tumor suppressor gene
-FGFR1 amplification

35
Q

squamous cell carcinoma - gross pathology

A

*large lesions, variegated color
*may have CENTRAL NECROSIS leading to CAVITATION

36
Q

squamous cell carcinoma - microscopic pathology

A

*sputum: orange-staining, keratinized squamous cells
*tissue:
-nests of polygonal cells with pink cytoplasm, distinct cell borders
-well differentiated = squamous KERATINIZING PEARLS
-poorly differentiated = anaplasia, pleomorphism, increased atypical mitoses

37
Q

keratin pearls are associated with what type of lung carcinoma

A

squamous cell carcinoma

38
Q

adenocarcinoma - overview

A

*malignant epithelial tumor with GLANDULAR DIFFERENTIATION and/or MUCIN PRODUCTION
*most common type in women, young patients, non-smokers
*arise more PERIPHERAL:
-bronchioles, alveoli
-produce fewer symptoms in early course of disease

39
Q

adenocarcinoma - pathogenesis

A

*less associated with tobacco smoking than other subtypes
*oncogenic mutations of growth factor receptor pathways (EGFR, ALK, ROS1)
-mutations are important for prognosis because there is targeted therapies

40
Q

adenocarcinoma - gross pathology

A

*tend to be smaller lesions
*may be solitary or multiple nodules
*may involve entire lobe, mimicking lobar pneumonia

41
Q

adenocarcinoma - microscopic pathology

A

*GLANDULAR EPITHELIAL CELLS +/- mucin
*peripheral lepidic pattern of spread = tumor cells “crawl” along normal-appearing alveolar septa
*need to determine mutations present to determine treatment

42
Q

large cell carcinoma - overview

A

*UNDIFFERENTIATED malignant epithelial tumor lacking features of other forms of lung cancer
*associated with smoking
*arise central OR peripheral

43
Q

large cell carcinoma - pathology

A

*large, polygonal ANAPLASTIC cells
-growing in sheets or solid nests
-foci of central necrosis and hemorrhage
*diagnosis of exclusion (no glandular/mucin, squamous, or neuroendocrine differentiation)

44
Q

small cell carcinoma - overview

A

*malignant neoplasm of PULMONARY NEUROENDOCRINE CELLS
-in physiologic states, these cells secrete serotonin, calcitonin, and gastrin-releasing peptide
-in tumors, secrete ACTH, other neuropeptides
*may arise in MAJOR BRONCHI or PERIPHERY
*MOST AGGRESSIVE OF LUNG TUMORS

45
Q

small cell carcinoma - pathogenesis

A

*exposure to carcinogens and other stimuli cause PEC proliferation
*virtually ALWAYS associated with exposure to tobacco smoke
*highest mutational burden among lung cancers (universal inactivation of both p53 and RB; loss of chromosome 3p also occurs)

46
Q

small cell carcinoma - gross pathology

A

*arising centrally
*may cause obstruction of main bronchus or spread along the bronchi (peribronchial spread)

47
Q

small cell carcinoma - microscopic pathology

A

*small cells with scant cytoplasm, ill-defined cell borders
-nuclear molding prominent
-fine chromatin “salt and pepper”
*sheet of tiny blue cells
*numerous mitoses
*extensive necrosis

*NO glandular or squamous differentiation

48
Q

lung carcinoma: metastases

A

*systemic metastatic spread of lung neoplasm
*lung carcinomas have predilection to metastasize
*hematogenous or direct extension
*sites:
-BRAIN / leptomeningeal (small cell carcinoma, adenocarcinoma)
-bone/bone marrow
-adrenal gland: (non-small cell carcinomas)

49
Q

metastatic disease of lung

A

*lung is most common site of metastatic neoplasms (more common than primary lung neoplasms)
*hematogenous spread, lymphatic spread, or direct extension
*variable patterns:
-multiple: “cannonball lesions” scattered throughout
*biopsy recapitulates the neoplasm of origin (ex. if metastatic colon cancer, it will look like colon pathology)

50
Q

mesothelioma - overview

A

*malignant epithelial neoplasm of MESOTHELIAL CELL ORIGIN
*history of ASBESTOS EXPOSURE (direct or secondary)
*arise in PARIETAL OR VISCERAL PLEURA
-tumor usually encases lung

51
Q

mesothelioma - pathogenesis

A

*asbestosis with long latency period after initial exposure, 25-40 years later
*asbestos preferentially accumulate in subpleural alveoli near mesothelial cell layer
*induce production of ROS, leading to DNA damage and multiple driver mutations

52
Q

mesothelioma - gross pathology

A

*preceded by pleural fibrosis/plaque
*dense white encircling tumor mass:
-big bulky tumors filling chest cavity
-obliterates pleural cavity

53
Q

mesothelioma - microscopic pathology

A

*microscopic appearance is variable:
-epithelial (left) = carcinomatous appearance
-spindle (right) = sarcomatous appearance
-biphasic = epithelial + spindle

Pulmonology Exam (36 decks)

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