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Pathology > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What is atelectasis?

A

area of airless pulmonary parenchyma, due to collapse or incomplete expansion

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2
Q

Describe the different types of atelectasis.

A

1) resorption: complete obstruction, collapse / mediastinum shifts towards affected lung
2) compression: fluid, tumor, or air accumulates in pleural space preventing expansion / mediastinum shifts away from affected lung
3) Contraction: pulmonary or pleural fibrosis prevents expansion / not reversible

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3
Q

Types of pulmonary edema?

A

hemodynamic
secondary to microvascular injury

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4
Q

what is hemodynamic pulmonary edema?

A
  • intra-alveolar fluid accumulation due to increased hydrostatic pressure in pulmonary circulation
  • hemosiderin-laden macrophages within alveoli with chronic edema
  • decreased oxygenation & increased chance of infection
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5
Q

Describe pulmonary secondary to microvascular injury.

A
  • injury to & inflammation of alveolar vascular endothelium or respiratory epithelium
  • infectious or toxic insults
  • localized or diffuse
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6
Q

Describe what obstructive lung disease are characterized by.

A

increase in resistance to airflow due to obstruction at any level from trachea to respiratory bronchioles
–> decreased maximal flow rates during forced expiration **

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7
Q

Examples of obstructive lung dx?

A
  • emphysema
  • chronic bronchitis
  • asthma
  • bronchiectasis
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8
Q

What diseases typically go together to makeup COPD?

A

chronic bronchitis & emphysema

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9
Q

Risk factors / susceptibility for COPD?

A
  • women & african americans
  • smokers (80% due to smoking)
  • environmental/occupational pollutants
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10
Q

Describe emphysema.

A
  • destruction of airway walls & irreversible enlargement of airways distal to terminal bronchiole
  • classified by site of involvement within pulmonary acinus
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11
Q

What is centriacinar emphysema?

A
  • predominantly heavy smokers
  • respiratory bronchioles involved (spares distal alveoli)
  • more lesions in upper/apical segments
  • patchy distribution
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12
Q

describe panacinar emphysema?

A
  • associated with alpha-antitrypsin deficiency
  • alveoli distal to respiratory bronchioles involved
  • more lesions in lower/anterior aspects (bases)
  • more evenly distributed
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13
Q

What is alpha 1 antitrypsin?

A

protease inhibitor –> especially elastase (destructive)
**homozygotes have significant decrease in protease inhibitor & 80% develop panacinar emphysema

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14
Q

Pathogenesis of emphysema/alveolar wall destruction?

A
  • exposure to particles in tobacco stimulates inflammation (IL8, TNF)
  • imbalance of proteases / antiproteases
  • oxidative stress (smoke, inflammatory cell products)
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15
Q

How is emphysema an obstructive dx?

A

small airways no longer held open by elastic recoil –> collapse during expiration

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16
Q

Clinical course of emphysema?

A
  • no symptoms until 1/3 lung tissue affected
  • initial symptoms: dyspnea, cough, & WHEEZING
  • severe: barrel chest, weight loss, prolonged expiration
  • may progress to pulmonary HTN & RHF
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17
Q

Why do people die due to emphysema?

A

respiratory failure
RHF
pneumothorax –> lung collapse

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18
Q

What describes chronic bronchitis?

A

chronic, persistent productive cough without any other identifiable cause

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19
Q

Pathogenesis of chronic bronchitis?

A
  • initiating factor = exposure of bronchi to inhaled irritants
  • mucus hypersecretion
  • chronic inflammation –> damage & fibrosis in small airways
  • diminished ciliary action = stasis of mucus
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20
Q

Chronic bronchitis morphological changes?

A
  • edema & swelling of respiratory mucosa (often squamous metaplasia)
  • hyperplasia of submucosal mucous glands of trachea & larger bronchi (thickness of mucus gland layer increases)
  • increased goblet cells in small bronchi & bronchioles, & extensive small airway mucous plugging
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21
Q

Clinical course of chronic bronchitis?

A
  • persistent productive cough
  • dyspnea on exertion
  • hypercapnia, hypoxia, mild cyanosis
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22
Q

What is characteristic of asthma?

A
  • chronic disorder of conducting airways:
    –> recurrent bronchoconstriction
    –> inflammation of bronchial walls
    –> increased mucus secretion
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23
Q

Symptoms of asthma?

A
  • recurrent wheezing, shortness of breath/chest tightness, cough
  • more frequent at night/early morning
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24
Q

What is atopic asthma?

A
  • Type I (IgE) hypersensitivity rxn
  • usually childhood onset
  • triggered by allergens
    –> pt with high serum IgE & + skin test for allergen, often family hx
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25
Q

Pathogenesis of atopic asthma?

A
  • sensitization with Th2 cell after antigen presentation stimulates IgE production & recruits eosinophils, stimulates mucus production
  • IgE binds to Fc receptors on mast cells
  • re-exposure cross links IgE molecules on mast cells –> degranulation & hypersensitivity rxn
    –> immediate & late phase
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26
Q

Immediate phase reaction?

A
  • minutes
  • bronchoconstriction
  • mucus secretion
  • increased vascular permeability
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27
Q

Late phase reaction?

A
  • hours
  • recruit more inflammatory cells
  • damage to mucosal tissue
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28
Q

What is non-atopic asthma?

A
  • bronchoconstriction triggered by stimuli:
    –> viruses, irritants, cold air, exercise
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29
Q

Morphologic changes of repeated allergen exposure induced airway remodeling?

A
  • smooth muscle hypertrophy/plasia
  • subepithelial fibrosis
  • submucosal gland hyperplasia
  • increased airway vascularity
  • increased thickness of airway wall*
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30
Q

What are Curschmann spirals?

A

in severe cases of asthma, bronchiole occluded with thick mucus plugs

31
Q

What are Charcot-Leydon crystals?

A

from degranulated eosinophils

32
Q

What is bronchiectasis?

A
  • chronic, recurrent necrotizing infections that eventually destroy smooth muscle & elastic tissue leading to permanent dilation of bronchi
  • impedance of normal drainage
33
Q

Predisposing conditions for bronchiectasis?

A
  • conditions affecting mucus clearing (CF, primary ciliary dyskinesia, bronchial obstruction)
34
Q

Repeated attempts to resolve the inflammatory process from bronchiectasis may result in?

A

peribronchial fibrosis

35
Q

List chronic diffuse interstitial (restrictive) dx of lungs?

A
  • pneumoconiosis
  • coal worker’s lung dx
  • silicosis
  • asbestos-related
36
Q

What are pneumoconioses?

A
  • nontumor lung dx after exposure to mineral dusts, particles, fumes
37
Q

Pathogenicity of particles are influenced by?

A
  • size (1-5 um most pathogenic)
  • particle solubility (more soluble = acute / less = chronic)
  • level/duration of exposure
  • intensity of immune response
38
Q

What is coal worker’s lung dx?

A
  • inhaled CARBON dust taken up by macrophages accumulates in IF along pulmonary lymphatic tissue
39
Q

what is anthracosis?

A

black pigmented lesions from coal dust macrophages
–> also seen in smokers & urban dwellers
–> can cause centriacinar emphysema

40
Q

Complicated coal workers’ pneumoconiosis can lead to?

A
  • progressive massive fibrosis
    –> multiple scars that can lead to RHF, pulmonary HTN, resp. failure
41
Q

What is silicosis?

A
  • inhaling crystallin silicon dioxide over long periods of time ingested by macrophages
  • most common occupational dx worldwide
42
Q

Morphology of silicosis?

A
  • slow growing collagenous nodular scars in lungs or hilar lymph nodes
    –> whorled balls of dense collagen surrounded by dust-containing macrophages
    *initially more prominent apically
    –> particles light up with plane-polarized light
  • may coalesce –> progressive massive fibrosis
43
Q

Clinical course of silicosis?

A
  • rate / progression highly variable
  • increased susceptible to TB
  • 2x risk of lung cancer
44
Q

What is asbestos related pulmonary dx?

A
  • fibrous hydrated silicate crystals cause interstitial & pleural fibrosis & lead to lung carcinoma & malignant mesothelioma
  • may result in honeycomb lung
  • presence of asbestos/ferruginous bodies (beads on a string)
  • plaques of dense collagen, sometimes calcified on pleura (parietal) –> often asymptomatic
  • may result in pleural effusion
45
Q

Community acquired bacterial pneumonia?

A
  • may be indistinguishable from viral clinically & radiologically
  • may follow viral URI
46
Q

Predisposing factors to community acquired bacterial pneumonia?

A
  • young or old
  • chronic dx (COPD, diabetes, CHF)
  • absent splenic fx
47
Q

Which bacteria that cause community acquired bacterial pneumonia do we have vaccines for?

A
  • S. pneumoniae (most common)
  • Haemophilus influenzae (pediatric)
    (bc encapsulated)
48
Q

Which bacteria spreads through blood vessels?

A
  • Pseudomonas aeruginosa
49
Q

Morphologic changes of pneumonia?

A
  • invasion of bacteria leads to alveolar filling with inflammatory cells & exudate
  • results in consolidation (solidification) of lung tissue
    –> bronchopenumonia
    –> lobar pneumonia
50
Q

What is bronchopneumonia?

A
  • patchy involvement of lung
  • areas may coalesce
  • acute suppuration
  • Basal, often Multilobular or bilateral
51
Q

What is lobar pneumonia?

A
  • consolidation of entire lobe
  • four stages:
    –> congestion: engorgement & fluid filled alveoli/bacteria
    –> red hepatization: exudate with neutrophils, RBC, fibrin
    –> grey hepatization: fibrinosuppurative, RBC disintegration, early organization
    –> resolution: organizing fibrosis with macrophages
52
Q

Clinical course of bacterial pneumonia?

A
  • abrupt fever, chills, productive cough (rust colored sputum)
  • lobar pneumonia: opaque lobe
  • broncho pneumonia: focal opacities
  • antibiotics (culture for specificity)
  • Complications: abscess, empyema, bacteremia
53
Q

Viral pneumonia common organisms?

A
  • influenza A*, B, C
  • RSV
  • human metapneumovirus
  • adenovirus
  • rhinovirus
  • coronavirus
54
Q

Variable clinical course of COVID-19?

A
  • cytokine storm
  • arterial or venous thrombosis
55
Q

Why does influenza cause epidemics/pandemics?

A
  • can infect may animals –> antigenic shift via recombination when coinfected = new strain / pandemic
  • 8 rna segments
  • rna polymerase lacks error detection leading to antigenic drift
56
Q

Course of TB infection?

A
  • airborne droplet
  • enter macrophage, replicates, bacteremia & seeding in multiple sites
  • macrophages activated (cell mediated) & tissue hypersensitivity
  • granulomatous inflammation
57
Q

What is a Gohn complex?

A
  • focus in lung parenchyma with consolidation & necrosis // scarring
  • caseating necrosis
    **primary TB infection
58
Q

What is secondary TB?

A
  • previously sensitized host from dormant lesions
  • typically apices of lungs
  • spread through blood = miliary TB: liver, bone marrow, spleen, adrenal glands
  • isolated organ TB from seeding
59
Q

What organisms cause hospital acquired pneumonia?

A
  • Enterobacteriaceae
  • pseudomonas (often from ventilator)
  • S. aureus
60
Q

Squamous cell carcinoma ?

A
  • strong association with tobacco smoke
  • high frequency of p53 mutation & overexpression
  • arise in Central lung/hilar region
61
Q

What is adenocarcinoma?

A
  • smokers or NONsmokers*
  • more likely peripheral
  • gain of function mutations (GF receptor pathways)
  • precursor lesions (hyperplasia/in situ)
62
Q

Small cell carcinom?

A
  • strongest association with SMOKING
  • frequent TP53 & RB mutations
  • aggressive, very high Fatality
  • central or peripheral –> likely from neuroendocrine cells in bronchial epithelium
63
Q

Appearance of small cell carcinoma?

A
  • small tumor cells with little cytoplasm
  • closely arranged nuclei with “molding” & absent nucleoli
  • grow in clusters without pattern
    *necrosis possible
64
Q

Large cell carcinoma?

A
  • poorly differentiated subtype of NSCC, without neuroendocrine, squamous, or glandular differentiation
    *diagnosis of exclusion
65
Q

Where does metastasis for lung cancer typically occur?

A

> 50% adrenal glands
30-50% liver
20% brain & bone

66
Q

Tumors metastatic to lung mainly originate?

A
  • breast
  • colon
  • kidney
  • prostate
  • bladder
67
Q

Carcinoid tumor?

A
  • arise from bronchial neuroendocrine cells
  • low grade malignant neoplasm
  • central or peripheral
  • nests of regular cells
    *atypical carcinoids show more variability / more likely to invade
68
Q

Symptoms of carcinoid tumor?

A
  • related to bronchial obstruction: coughing, hemoptysis, impaired drainage
  • secrete vasoactive amines (serotonin): flushing, diarrhea, cyanosis
69
Q

5 year survival rate for typical carcinoids/atypical?

A

95% / 70%

70
Q

Malignant mesothelioma?

A
  • increased incidence with asbestos exposure compounded with smoking
  • most common homozygous deletion of p16
  • arises from pleura & spreads into pleural space unsheathing & compressing lung
  • epithelioid or sarcomatoid
    *may invade adjacent structures
71
Q

Presentation of malignant mesothelioma?

A

chest pain, dyspnea,, recurrent pleural effusions

72
Q

Survival rate for MM?

A

1 year ~50%, most do not survive 2yrs

73
Q

Squamous papilloma of larynx?

A
  • squamous filled fronts with fibrovascular cores
  • single or multiple
    **HPV6 & 11
  • benign, but may recur
74
Q

Laryngeal carcinoma?

A
  • SCC typical in men, 50s, smokers
  • arise from dysplastic squamous epithelium
  • often forms bulky, fungating mass protruding from surface, often ulcerated

Pathology (9 decks)

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