Respiratory Flashcards
1
Q
What is atelectasis?
A
area of airless pulmonary parenchyma, due to collapse or incomplete expansion
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
3
Q
Types of pulmonary edema?
A
hemodynamic
secondary to microvascular injury
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
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
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 **
7
Q
Examples of obstructive lung dx?
A
- emphysema
- chronic bronchitis
- asthma
- bronchiectasis
8
Q
What diseases typically go together to makeup COPD?
A
chronic bronchitis & emphysema
9
Q
Risk factors / susceptibility for COPD?
A
- women & african americans
- smokers (80% due to smoking)
- environmental/occupational pollutants
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
11
Q
What is centriacinar emphysema?
A
- predominantly heavy smokers
- respiratory bronchioles involved (spares distal alveoli)
- more lesions in upper/apical segments
- patchy distribution
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
13
Q
What is alpha 1 antitrypsin?
A
protease inhibitor –> especially elastase (destructive)
**homozygotes have significant decrease in protease inhibitor & 80% develop panacinar emphysema
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)
15
Q
How is emphysema an obstructive dx?
A
small airways no longer held open by elastic recoil –> collapse during expiration
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
17
Q
Why do people die due to emphysema?
A
respiratory failure
RHF
pneumothorax –> lung collapse
18
Q
What describes chronic bronchitis?
A
chronic, persistent productive cough without any other identifiable cause
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
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
21
Q
Clinical course of chronic bronchitis?
A
- persistent productive cough
- dyspnea on exertion
- hypercapnia, hypoxia, mild cyanosis
22
Q
What is characteristic of asthma?
A
- chronic disorder of conducting airways:
–> recurrent bronchoconstriction
–> inflammation of bronchial walls
–> increased mucus secretion
23
Q
Symptoms of asthma?
A
- recurrent wheezing, shortness of breath/chest tightness, cough
- more frequent at night/early morning
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
25
Pathogenesis of atopic asthma?
- 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
26
Immediate phase reaction?
- minutes
- bronchoconstriction
- mucus secretion
- increased vascular permeability
27
Late phase reaction?
- hours
- recruit more inflammatory cells
- damage to mucosal tissue
28
What is non-atopic asthma?
- bronchoconstriction triggered by stimuli:
--> viruses, irritants, cold air, exercise
29
Morphologic changes of repeated allergen exposure induced airway remodeling?
- smooth muscle hypertrophy/plasia
- subepithelial fibrosis
- submucosal gland hyperplasia
- increased airway vascularity
- increased thickness of airway wall*
30
What are Curschmann spirals?
in severe cases of asthma, bronchiole occluded with thick mucus plugs
31
What are Charcot-Leydon crystals?
from degranulated eosinophils
32
What is bronchiectasis?
- chronic, recurrent necrotizing infections that eventually destroy smooth muscle & elastic tissue leading to permanent dilation of bronchi
- impedance of normal drainage
33
Predisposing conditions for bronchiectasis?
- conditions affecting mucus clearing (CF, primary ciliary dyskinesia, bronchial obstruction)
34
Repeated attempts to resolve the inflammatory process from bronchiectasis may result in?
peribronchial fibrosis
35
List chronic diffuse interstitial (restrictive) dx of lungs?
- pneumoconiosis
- coal worker's lung dx
- silicosis
- asbestos-related
36
What are pneumoconioses?
- nontumor lung dx after exposure to mineral dusts, particles, fumes
37
Pathogenicity of particles are influenced by?
- size (1-5 um most pathogenic)
- particle solubility (more soluble = acute / less = chronic)
- level/duration of exposure
- intensity of immune response
38
What is coal worker's lung dx?
- inhaled CARBON dust taken up by macrophages accumulates in IF along pulmonary lymphatic tissue
39
what is anthracosis?
black pigmented lesions from coal dust macrophages
--> also seen in smokers & urban dwellers
--> can cause centriacinar emphysema
40
Complicated coal workers' pneumoconiosis can lead to?
- progressive massive fibrosis
--> multiple scars that can lead to RHF, pulmonary HTN, resp. failure
41
What is silicosis?
- inhaling crystallin silicon dioxide over long periods of time ingested by macrophages
- most common occupational dx worldwide
42
Morphology of silicosis?
- 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
Clinical course of silicosis?
- rate / progression highly variable
- increased susceptible to TB
- 2x risk of lung cancer
44
What is asbestos related pulmonary dx?
- 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
Community acquired bacterial pneumonia?
- may be indistinguishable from viral clinically & radiologically
- may follow viral URI
46
Predisposing factors to community acquired bacterial pneumonia?
- young or old
- chronic dx (COPD, diabetes, CHF)
- absent splenic fx
47
Which bacteria that cause community acquired bacterial pneumonia do we have vaccines for?
- S. pneumoniae (most common)
- Haemophilus influenzae (pediatric)
(bc encapsulated)
48
Which bacteria spreads through blood vessels?
- Pseudomonas aeruginosa
49
Morphologic changes of pneumonia?
- invasion of bacteria leads to alveolar filling with inflammatory cells & exudate
- results in consolidation (solidification) of lung tissue
--> bronchopenumonia
--> lobar pneumonia
50
What is bronchopneumonia?
- patchy involvement of lung
- areas may coalesce
- acute suppuration
- Basal, often Multilobular or bilateral
51
What is lobar pneumonia?
- 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
Clinical course of bacterial pneumonia?
- 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
Viral pneumonia common organisms?
- influenza A*, B, C
- RSV
- human metapneumovirus
- adenovirus
- rhinovirus
- coronavirus
54
Variable clinical course of COVID-19?
- cytokine storm
- arterial or venous thrombosis
55
Why does influenza cause epidemics/pandemics?
- 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
Course of TB infection?
- airborne droplet
- enter macrophage, replicates, bacteremia & seeding in multiple sites
- macrophages activated (cell mediated) & tissue hypersensitivity
- granulomatous inflammation
57
What is a Gohn complex?
- focus in lung parenchyma with consolidation & necrosis // scarring
- caseating necrosis
**primary TB infection
58
What is secondary TB?
- 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
What organisms cause hospital acquired pneumonia?
- Enterobacteriaceae
- pseudomonas (often from ventilator)
- S. aureus
60
Squamous cell carcinoma ?
- strong association with tobacco smoke
- high frequency of p53 mutation & overexpression
- arise in Central lung/hilar region
61
What is adenocarcinoma?
- smokers or NONsmokers*
- more likely peripheral
- gain of function mutations (GF receptor pathways)
- precursor lesions (hyperplasia/in situ)
62
Small cell carcinom?
- strongest association with SMOKING
- frequent TP53 & RB mutations
- aggressive, very high Fatality
- central or peripheral --> likely from neuroendocrine cells in bronchial epithelium
63
Appearance of small cell carcinoma?
- small tumor cells with little cytoplasm
- closely arranged nuclei with "molding" & absent nucleoli
- grow in clusters without pattern
*necrosis possible
64
Large cell carcinoma?
- poorly differentiated subtype of NSCC, without neuroendocrine, squamous, or glandular differentiation
*diagnosis of exclusion
65
Where does metastasis for lung cancer typically occur?
>50% adrenal glands
30-50% liver
20% brain & bone
66
Tumors metastatic to lung mainly originate?
- breast
- colon
- kidney
- prostate
- bladder
67
Carcinoid tumor?
- 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
Symptoms of carcinoid tumor?
- related to bronchial obstruction: coughing, hemoptysis, impaired drainage
- secrete vasoactive amines (serotonin): flushing, diarrhea, cyanosis
69
5 year survival rate for typical carcinoids/atypical?
95% / 70%
70
Malignant mesothelioma?
- 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
Presentation of malignant mesothelioma?
chest pain, dyspnea,, recurrent pleural effusions
72
Survival rate for MM?
1 year ~50%, most do not survive 2yrs
73
Squamous papilloma of larynx?
- squamous filled fronts with fibrovascular cores
- single or multiple
**HPV6 & 11
- benign, but may recur
74
Laryngeal carcinoma?
- SCC typical in men, 50s, smokers
- arise from dysplastic squamous epithelium
- often forms bulky, fungating mass protruding from surface, often ulcerated
