L2- Pulmonary Pathology I Flashcards
Define the following:
- TV
- IRV
- ERV
- RV
Tidal Vol.: volume of air inhaled and exhaled with normal respiration
Inspiratory Reserve Vol.: volume of air that can be inhaled beyond normal inspiration
Expiratory Reserve Vol.: volume of air that can be exhaled beyond normal expiration
Residual Vol.: left over air volume after maximal exhalation
Define the following:
- TLC
- VC
- IC
- FRC
Total Lung Capacity: maximal lung volume after maximal inhalation
Vital Capacity: maximal lung volume that can be inhaled/exhaled (TLC - RV = IRV + ERV + TV)
Inspiratory Capacity: maximal air volume that can be inhaled following normal expiration (TV + IRV)
Functional Residual Capacity: lung volume after normal expiration (ERV + RV)
Define the following:
- FVC
- FVC1
- FEF
Forced Vital Capacity: volume of air exhaled with force following maximal inhalation
FVC-1: volume of air exhaled with force in first second following maximal inhalation
Forced Expiratory Flow (25%-75%): measure of airflow midway through expiration (middle half)
Describe how the following change in Restrictive Lung Disease:
- FEV1/FVC
- FEV1
- FVC
- TLC
- FEV1/FVC: normal or inc (>80%)
- FEV1: normal or slightly dec
- FVC: dec
- TLC: dec
Describe how the following change in Obstructive Lung Disease:
- FEV1/FVC
- FEV1
- FVC
- TLC
- FEV1/FVC: dec (<70%)
- FEV1: dec (significant)
- FVC: dec or normal
- TLC: inc or normal
list the 4 types of laboratory tests conducted in the respiratory system
- Sputum analysis: cells, microbiology
- Arterial blood gases (pCO2, pO2)
- Pleural fluid
- Blood Culture
describe the goal or types of tests conducted in sputum analysis
Cell analysis: WBCs, RBCs, malignant cells
Microbiological Studies:
- bacteria (staining, culture, AB resistant)
- fungal (KOH, culture)
- viral (PCR, DNA, culture)
- NAAT (nucleic acid amplification testing)
what are the blood gas changes seen in lung diseases and why are they monitored
- pCO2: looking for INCreases
- pO2: looking for DECreases
-the quantity of changes determines the severity of the disease progression
describe how pleural fluid is studied for lung diseases
-used as a therapeutic or diagnostic technique
i) Cell Count: HF (dec to normal) vs Infection (inc)
ii) Malignancy: primary vs secondary
list the techniques or procedures used to acquire lung sample for cytology (hint- 9)
- bronchial washings (inject slime and aspirate it out)
- bronchial brushing (scraping lesion)
- TBNA, transbronchial needle aspiration
- TTNA, transthoracic needle aspiration
- EBUS-FNA, endobronchial ultrasound-guided fine needle aspiration
-navigational bronchoscopy
- bronchoscopic biopsy: transbronchial, endobronchial
- pleuroscopic biopsy
-Surgical biopsy / resection: VATS (video assisted transthoracic) biopsy or Open biopsy
foreign objects that are accidentally inhaled will generally go into the (R/L) lung because of (2)
R lung- the R main bronchus is shorter and more vertical than the L
Respiratory Zone function, (1)
Conducting Zone function, (2)
1- gas exchange
2- carry, warm, filter, humidify air
list the components of the Bronchial Walls (histology)
[conducting zone only- no gas exchange] (inside to outside) 1) Epithelium: ciliated columnar cells, goblet cells, basal cells, neuroendocrine cells 2) Basement Membrane 3) Smooth Muscle 4) Seromucinous Glands 5) Cartilage 6) Vasculature and Lymphatics
list the components of the Bronchiolar Walls (histology)
[conducting zone until terminal bronchioles –> respiratory zone and respiratory bronchioles]
(inside to outside)
1) Epithelium: ciliated columnar cells, Clara cells
2) Basement Membrane
3) Smooth Muscle
4) Vasculature and Lymphatics
compare the epithelium of Bronchi and Bronchioles
Bronchi: ciliated columnar cells, goblet cells, basal cells, neuroendocrine cells
Bronchioles: ciliated columnar cells, Clara cells
describe the histology of alveoli
(inside to outside)
1) epithelium: type I/II pneumocytes
2) alveolar macrophages
3) interstitium
4) capillaries (endothelial cells)
The alveolar epithelium is mostly type (I/II) pneumocytes.
- type I function, (2)
- type II function, (3)
1- type I, 95%
2- gas exchange
3- surfactant production, alveolar epithelium repair (generates type I and II pneumocytes)
______ cells are responsible for gas exchange in alveoli
type I pneumocytes
______ cells are responsible for surfactant production
type II pneumocytes
______ cells are responsible for repairing alveolar epithelium
type II pneumocytes (generates type I and II pneumocytes)
Atelectasis refers to either (1) or (2). The loss of (3) is secondary to (1)/(2) and has the following progression, (4).
(atelectasis = collapsed lung)
1- incomplete expansion of lungs (neonatal atelectasis)
2- collapse of previously inflated lung
3- lung volume
4- dec oxygenation –> ventilation perfusion imbalance
list the three types of atelectasis
(based on cause and mechanism)
- resorption atelectasis (obstruction)
- compression atelectasis
- contraction atelectasis
(1) atelectasis results do to some obstruction as a result of one of the following, (2)
Resorption Atelectasis
- mucus/mucopurulent plug post-surgery
- aspiration of foreign material
- bronchial asthma, chronic bronchitis, bronchiectasis
- bronchial neoplasms (if total obstruction)
Resorption atelectasis results from (1) of the (2) part of respiratory tract. As a result, (3) is prevented and the (4) progression will occur to cause final (5) change to the lung.
1- complete obstruction
2- bronchi, subsegemental bronchi, bronchioles
3- airflow to alveoli
4- trapped air in distal spaces is resorbed thru Pores of Kohn (alveoli to alveoli) –> lack of air to distal airspaces –> (5)
5- lung collapse
In resorption atelectasis, (1) is evident or presents 24-36 hrs post-lung collapse.
- (2) and (3) are evident on imaging (X-Ray)
- (4) is evident upon palpation and auscultation
1- fever, dyspnea
2- ipsilateral deviation of trachea / mediastinum
3- ipsilateral diaphragmatic elevation
4- absent breath sounds (no expansion upon inspiration –> dec air movement) + absent vocal vibratory sensation / tactile fremitus
Compression atelectasis or lung collapse can occur due to accumulation of…… (include examples)
- air
- fluid
- tumor
i.e. tension pneumothorax, pleural effusion
_________ is the main clinical feature of compression atelectasis
(contralateral) trachea and mediastinum shift away from affected lung
Contraction atelectasis, aka (1), occurs due to (2) affecting (3) or (4) which will prevent (5)
1- cicatrization atelectasis 2- fibrosis (local or diffuse) 3- lung 4- pleura 5- lung expansion
(T/F) atelectasis is a reversible process
T- Resorption and Compression atelectasis
F- Contraction atelectasis
atelectasis is treated promptly in order to prevent….
- hypoxemia
- superimposed infection of collapsed lung
Surfactant is made out of….
(lipoprotein)
Lipids: phosphatidylcholine (lecithin), phosphatidylglycerol
Surfactant Proteins: SP- A, B, C, D
surfactant production begins during (1) and is stored in (2)
1- week 28 of gestation
2- lamellar bodies of type II pneumocytes
- surfactant production is increased in response to (1) hormone(s)
- surfactant production is decreased in response to (2) hormone(s)
1- (inc) cortisol, thyroxine
2- (dec) insulin
describe the function of SP- A, B, C, D
(surfactant protein)
B, C: reduces surface tension at air-liquid barrier in alveoli –> prevents collapse on expiration
A, D: innate immunity
SP-__ functions in the innate immune system
Surfactant Protein- A, D
SP-__ functions to reduce air-liquid barrier surface tension to prevent lung collapse upon expiration
Surfactant Proteins- B, C
Neonatal atelectasis causes (1) in newborns and occurs as a result from (2).
Risk factors: (3), (4), (5)
1- RDS (respiratory distress syndrome)
2- dec surfactant production
3- premature birth: before 28 wks
4- maternal diabetes: fetal hyperglycemia => insulin release => dec production
5- C-section: b/c dec cortisol => dec production // labor/vaginal delivery inc stress => inc production
how does maternal diabetes affect surfactant production
- fetal hyperglycemia => insulin release
- insulin dec surfactant production
compare mechanism for increased surfactant production in vaginal delivery vs C-section
- vaginal birth => inc stress => inc cortisol => inc surfactant production
- C-section has less cortisol in neonate, less surfactant production
Neonatal atelectasis results in hypoxemia and CO2 retention in the body, which is mainly exhibited by (1) in the blood. As a result of (1), (2) occurs which causes (3) and (4), where (2), (3), (4) all compound the hypoxemia and CO2 retention. The biggest consequence of (3) and (4) is (5).
1- respiratory acidosis
2- pulmonary vasoconstriction / hypoperfusion
3- endothelial damage
4- epithelial damage
5- plasma leaks into alveoli –> hyaline membrane of fibrin and necrotic cells
_____ is the main histological feature of neonatal atelectasis
hyaline membrane (fibrin and necrotic cells) as a result of plasma leak into alveoli
Neonatal atelectasis is evident by (1) at birth, with (2) evident in blood work and (3) evident on imaging
1- RDS (respiratory distress syndrome) w/in few hrs of birth
2- hypoxemia, respiratory acidosis
3- ‘ground glass appearance’ (CXR)
list the common complications of neonatal atelectasis
- (1) in the brain
- (2) in the GIT
- (3) blood labs
- (4) blood vessel structure
- (5) as a result of Tx / therapy
1- intraventricular hemorrhage
2- necrotizing enterocolitis b/c intestinal ischemia
3- hypoglycemia b/c excessive insulin release
4- PDA b/c persistent hypoxemia
5- [via O2 therapy] lung damage (bronchopulmonary dysplasia) and cataracts/blindness
