Flashcards in Module 7 Pulmonary Deck (47):
Review: Explain TLC,RV,FVC,FEV and FEF
TLC: total lung capacity (lung volume following max inhalation)
RV: residual volume (volume following max exhalation)
FVC: forced vital capacity (volume exhaled with force following max inhalation)
FEV: forced expiratory volume (volume exhaled with force over a given period of time 1sec=FEV1)
FEF 25%-75%: forced expiratory flow (measure of airflow midway through exhalation)
Airway histology review: In bronchi what cells are present?
Epithelium: Ciliated columnar cells, goblet cells, basal cells (multipotent progenitor) and neuroendocrine cells (Chemoreceptors in hypoxia detection)
Vasculature and lymphatics
Airway histology review: In bronchioles what cells are present?
Epithelium: ciliated columnar cells and clara cells
vasculature and lymphatics
no cartilage or glands
Review: differentiate between type I and type II pneumocytes
type I: flat and can not replace itself; 95% of volume of alveoli are these cells
type II: larger, cuboidal, produce surfactant; can differentiate --- replaces injured epithelial (type I); located away from wall/gas diffusion
What structures are in the conduction, transition and respiratory zones?
Conduction zones: Bronchi and Bronchioles
Transition Zone: Respiratory Bronchioles
Respiratory zone: Alveoli ducts and Alveoli
What is atelectasis?
Alveolar collapse = loss of lung volume = decreased oxygenation ---- ventilation perfusion imbalance --- massive intrapulmonary shunting but normal blood flow
--caused by inadequate expansion of airspaces
There are three types of atelectasis each card will go through one. First is resorption (obstructive)
Resorption: obstruction of the bronchial lumen and this is reversible
--obstruction by either a FB (right main stem b/c its straight) , mucus plug or centrally located tumors
---xray: trachea goes to the same side as the obstruction
What are the different pathologies that cause mucus plugs that end up obstructing the lumen of the bronchus?
What are the different pathologies that cause centrally located tumors?
Squamous cell lung cancer, small cell carcinoma and Bronchial carcinoma
The second type of atelectasis is compression, what are the characteristics of this
Reversible and involves air or fluid in the pleural cavity:
--pneumothorax, hemothorax, penumohemothorax, chylothorax (lymph), empyema (pus) and pleural effusion
---xray: trachea is pushed to the opposite side (Not in the lab slides it shows a right sided pneumothorax so trachea goes to the left)
The third type of atelectasis is contraction, what are the characteristics of this?
Anything that causes pulmonary fibrosis and is therefore irreversible
--trachea is usually midline
---FEV:FVC ratio is normal but decreased TLC:RV
The next category of atelectasis is dealing with premature babies, what type of atelectasis is this?
Get microatelectasis because of lack of surfactant ( micro lung collapse) because very immature type 2 pneumocytes
In surfactant it is composed of lipoproteins, phosphatidylcholin (lecithin), Phosphatidylglycerol and proteins. What are the specific proteins and their associated functions
Surface proteins (SP) A and D: innate immunity
Surfactant proteins (SP) B and C: reduction of surface tension at air liquid barrier in alveoli
Surfactant is synthesized in type 2 pneumocytes, at how many weeks gestation does the surfactant start getting synthesized?
Synthesis begins by 28th weeks of gestation
Stored in lamellar bodies
Neonatal atelectasis is also known as respiratory distress syndrome (RDS) in newborns and again as already discussed this deals with decreased surfactant in fetal lungs. What three predisposing factors in the mother during pregnancy can lead the unborn infant to have decreased surfactant production?
Maternal Diabetes (fetal hyperglycemia stimulates insulin release)
C. section: labor and vaginal delivery leads to increased stress related cortisol secretion and therefore increased surfactant production
(remember that in regards to surfactant, synthesis is increased by cortisol and thyroxine and decreased by insulin)
Neonatal atelectasis has what clinical findings?
--resp distress within a few hours of birth
--hypoxemia and resp acidosis
--ground glass appearance on CXR
What are the systemic complications for neonatal atelectasis?
Patient ductus arteriosus (persistent hypoxemia)
Necrotizing enterocolitis (intestinal ischemia)
Hypoglycemia (Excessive insulin release)
O2 therapy (damage to lungs and cataracts)
What are the various names for Acute Respiratory Distress Syndrome (ARDS)?
Diffuse Alveolar damage
Hyaline Membrane Disease
Acute lung injury
What is included in the criteria for dx of ARDS?
---Sudden onset of symptoms (SOB, tachy, cyanosis, and tachypnea)
----Ground glass appearance on chest xray (because of diffuse pulmonary edema)
---pulmonary papillary wedge pressure is normal (this is non cardiogenic so therefore no left heart failure so entirely pulmonary)
---refractory hypoxemia (giving oxygen via face mask and patients are still blue)
Since placing a face mask on these patients (with ARDS) will not help with the hypoxemia, how do you save them??
Positive Pressure Mechanical ventilation that will actually push O2 through...but be careful dont wanna give to much O2 because you could cause free radical damage and O2 toxicity.
For the etiology of ARDS there are direct and indirect causes. What are these causes ?
Direct: gastric aspiration, atypical pneumonia, near drowning, pulmonary contusion due to blunt force trauma and smoke inhalation
Indirect: septicemia, acute pancreatitis and uremia
(note: uremia is also the most common systemic disorder causing pericarditis)
The pathogenesis for ARDS involves two phases an acute (Exudative) phase and organizing (proliferative phase), explain the factors involved in the acute phase.
Acute (exudative) phase: 0-4 days
---direct or indirect damage to either type II pneumocytes or alveolar endothelial cells and those release IL-8 and these recruit PMNs and the PMNs secrete CCL2 which attracts macrophages
--lungs are heavy and firm
--Hyaline membrane (Composed of fibrin thats why it looks pink and its a diffusion barrier and its a fibrinous exudate)
--exudate is just WBCs and fibrin
--most patients will die during this phase
The next phase of ARDS is the organizing (proliferative phase), explain the factors involved in this phase
Organizing (proliferative) phase: 4days-3 weeks
--if patients are still alive (most will die in the first 24 hours) then
---proliferation of type II cells and organizing of fibroblasts via TGFbeta and TGFbeta is secreted by macrophages
--alveolar septal thickening
What would you see on the arterial blood gas for ARSD patients?
Hypoxemia (low O2)
Hypercapnia (high CO2)
Resp Acidosis (low pH)
---dont forget you see hyaline membrane on histology
What are complications seen in ARSD?
Resp failure is gonna kill them because of diffusion barrier but if they survive then fibrosis in lung after 2 weeks
--leads to contraction atelectasis and cor pulmonale and nutmeg liver (Chronic passive congestion)
What are obstructive lung diseases?
2. Chronic Bronchitis
3. Asthma (only one that is reversible)
What is the spirometry results for all obstructive lung diseases?
Increased TLC, RV and FRC (get air in)
Decreased FEV1: normal FVC (cant get it out)
hypoxia, hypercapnia and resp acidosis
What is emphysema?
Loss of elastic recoil and collapse of airways during exhalation results in obstruction and air trapping
--permanent destruction and dilatation of airways distal to terminal bronchioles without fibrosis
There are 4 types of emphysema, each card will go through one. Centroacinar --
Centroacinar: resp bronchioles and upper lobes
--Have to be a smoker because normal levels of A1AT but elastase overwhelms the A1AT and causes damage to the elastic tissue
--so patients are usually over 50
--why upper lobes? smoke rises to the top
The second type of emphysema, is Panacinar, what are some features?
Panacinar: Involves entire acinus ( resp. bronchioles, alveolar walls, and alveolar sacs distal to bronchioles)
--genetic defect of PIZZ in A1AT on chr. 14
--Liver makes A1AT and it is misfolded so the A1AT backs up in the liver and causes liver cirrhosis as a child
---middle aged persons present with lower lobe panacinar
---if patient has the PIZZ genetic defect and is a smoker then panaciner presents in the 20s or 30s.
The third type of emphysema is irregular or paracicratricial, what are some features?
---only one with fibrosis and contraction atelectasis
The fourth type of emphysema is septal (distal acinar), what are some features?
Ruptures into pleural space----bullae and pneumothorax --- compression atelectasis
--closest to pleural space
How do patients with emphysema present?
Skinny (compensating and using accessory muscles to try and get the air out)
Barrel chested (lung hyperinflation and increased AP diameter)
Hunched over and breathing through pursed lips
--pink puffers: compensating early to prevent cyanosis and hypoxia
Prolonged expiration (pursed lips)
What does spirometry, ABG and CXR show on patients with emphysema?
Spirometry: low FEV1:FVC and High TLC:RV
CXR: hyper-inflated or hyperlucent lung fields with flat diaphragm
ABG: compensate so CO2 and pH normal and O2 slightly low but late onset emphysema is low O2 and high CO2 and low pH (resp. acidosis)
What do you see on histology of patients with emphysema?
Over distended alveolar spaces because of loss of elastic recoil
--pores of kohn are very wide so easy for lobar pneumonia to spread
--free floating alveolar septa and air spaces
What complications do you see in a patient with emphysema?
--Cor pulmonale (right heart failure secondary to a pulmonary HTN)
--Secondary polycythemia: long standing hypoxia the kidney are gonna compensate and start making EPO which drives erythropoiesis (just too many RBCs)
Chronic Bronchitis is the next obstructive lung disease, what is the criteria for clinical dx?
Productive cough of foul smelling, purulent sputum for 3 consecutive months for 2 consecutive years
What is the etiology for chronic bronchitis?
What is the pathogenesis in the bronchus for chronic bronchitis?
Squamous metaplasia, goblet cell hyperplasia, thickened BM, hypertrophy of bronchial smooth muscle and hypertrophy/hyperplasia of seromucinous glands
--hypersecretion of mucus
--Reid index elevated greater than 50%
What is the Reid index?
Ratio of thickness of submucosal gland to overall bronchial wall
--normally around 0.4
-in chronic bronchitis of bronchus: 0.5
What is the pathogenesis in the bronchioles for chronic bronchitis?
Fibrosis of the bronchial wall ---- luminal narrowing, metaplasia of goblet cells (stem cells become goblet cells)
---bronchiolitis obliterans (obliteration of lumen of bronchioles)
---only place where you see fibrosis and scarring in chronic bronchitis
(cells= chronic inflammation, lymphocytes, fibrocytes and macrophages, CD8+ T cells) (no eosinophils)
What is the presentation for a patient with chronic bronchitis?
Blue bloaters --- b/c decompensate early, cor pulmonale --- ascites and peripheral edema and cyanosis
What do you see on CXR, ABG and Spirometry for patients with chronic bronchitis?
CXR: pneumonia b/c no cilia and resorption atelectasis b/c mucus plugs blocking the bronchial lumen
ABG: Hypoxia, hypercapnia and resp acidosis
Spirometry: decreased FEV:FVC ratio and increased TLC:RV
What are complications for chronic bronchitis?
Resp failure early, cor pulmonale early, cardiac cirrhosis/nutmeg liver, resorption atelectasis, recurrent pneumonia ----- lung abscess ---- bronchiectasis
What do you see on gross examination of the lungs in patients with emphysema?
---Hyperinflated lungs +/- bulla (large sacs filled with air) formation.
---parenchyma has a moth-eaten appearance
--permanent airspace enlargement is diffuse
Review: What is the distinct feature of chronic bronchitis?
Hypersecretioon of mucus