Lecture 6.1 MJ slides Flashcards
List the types of atelectasis
1) Contraction atelectasis
2) Resorption atelectasis
3) Compression atelectasis
Reabsorption atelectasis:
1) Define it
2) When may it occur?
3) What happens?
1) Obstruction impairs air from reaching distal airways
s/p thoracic surgery > mucopurulent plugs
2) In children (FB aspiration)
3) Any air present (and now trapped) is absorbed over time; Alveoli collapse
Compression atelectasis:
1) What is it? Give examples
2) What is it caused by? Give examples
1) Accumulation of fluid, blood, or air within pleural cavity
Pleural effusion, pneumothorax
2) Failure to breath deeply
Pain, neuromuscular disease
Define ARDS
“Rapid onset of life-threatening respiratory insufficiency, severe arterial hypoxemia, +/- cyanosis”
ARDS:
1) What kind of disease is it?
2) What is occurring? What does this cause?
1) Airspace disease: occurring in the alveoli
2) Integrity of alveolar: capillary membrane is compromised by endothelial and epithelial injury
-This leads to “diffuse alveolar damage”
-Then fluid build up in the airspace!
How does ARDS happen? (7 steps)
Initial insult: Infxn, caustic substance, etc.
1) Inflammatory reaction initiated by variety of pro-inflammatory mediators
2) Synthesis of cytokines neutrophil chemotaxis + interlukin 1 and TNF sequestration and activation of neutrophils in pulmonary capillaries
3) PMNs now occupy vascular space, the interstitium, and alveoli
4) PMN release caustic products: ROSs, proteases
5) Vascular leaking occurs and there is a loss of surfactant
6) Fluid in the airspaces
7) Oxygen cannot diffuse readily through fluid: disease rapidly becomes refractory to 02 therapy
With ARDS, If the patient lives, they will take how long to return to normal pulmonary function? Describe
6 to 12 months; however, often there is long-term damage (25% of cases)
List some long term damage that can occur due to ARDS
1) Type II pneumocytes proliferate to attempt to regenerate the alveolar lining
2) Proliferation of interstitial cells and deposition of collagen triggered by macrophages and placed down fibroblasts
3) Fibrin-rich exudates organize into interalveolar fibrosis
4) Thickening of alveolar septa
5) Chronic poor gas exchange
6) Less compliant and expansive lungs
7) Chronic lung disease
Obstructive Dz:
1) What do FVC and FEV1 look like? Define each
2) What does this look like?
1) Forced vital capacity (FVC) is normal and expiratory flow rate (FEV1) is significantly decreased
FVC: how much air you can blow out
FEV1: how much air you blow out in the first second
2) Very long expiratory phase; the ratio of FEV1/FVC is decreased
Restrictive Dz:
1) What are FEV and expiratory flow like?
2) What does this look like?
3) What are the pt’s other stats?
1) FVC is reduced and the expiratory flow rate is also reduced
2) The person doesn’t fill their lungs, so they don’t blow out much. . . But what they do blow out comes out pretty easily
3) In the FEV1/FVC ratio both numbers go down, but the ratio is roughly equal!
Describe the pathology of COPD/emphysema type of obstructive lung disease
Inhaled smoke causes lung damage and inflammation:
1) Inflammatory mediators are initiated and inflammatory cells recruited
2) Inflammatory cells release protease
3) Protease breaks down connective tissues, in particular elastin
4) Acinar damage ensues, causing the bulging of the acinus
5) Alveoli are lost
6) Number of alveolar capillaries are diminished
7) Diffusing capacity and gas exchange are reduced
8) Also, without elastic tissue, small airways collapse during expiration
9) Outward airflow obstruction
How is chronic bronchitis defined?
Persistent productive cough for 3 consecutive months in at least 2 consecutive years
How do you get COPD/bronchitis type of obstructive disease?
1) Cigarette smoke induces hypertrophy of mucous glands in trachea and bronchi
2) Transcription of the mucin gene in bronchial epithelium occurs
3) There is also an increase in mucin-secreting goblet cells in epithelial surfaces of small bronchi and bronchioles
4) Mucous plugging of the bronchiolar lumen
-Smoke also induces inflammation via macrophages and neutrophils
5) Local tissue destruction
6) Fibrosis
In chronic bronchitis we see PMNs and macrophages, but not eosinophils, which are the hallmark of what?
Asthma
1) Chronic bronchitis pts can also experience inflammation where?
2) What can sufferers of severe bronchiolitis experience?
1) In the small bronchi–bronchioles.
2) Complete fibrotic obstruction, termed “bronchiolitis obliterans”
List and describe the 2 main categories of long-term smoking effects
1) Neutrophils are recruited
- Elastase is produced
- Acini are damaged
2) Transcription of mucin gene
- Mucus plugging of bronchial lumen
- Inflammation and fibrosis
-There is almost always significant disease overlap in both types of COPD.
Asthma Pathology atopic type:
Excessive helper T cell activation releases cytokines, including which 3? Describe what each does
IL 5 > Mast Cells
IL 4 > IgE production > IgE coats the mast cells
IL 13 > mucous production > cough
Describe the early phase of atopic asthma and each of its two aspects
1) Coated mast cells encounter antigen and release histamine along with pro-inflammatory prostaglandin, and leukotrienes
a) Histamine > bronchospasm > wheezing
b) Leukotrienes > additional bronchoconstriction
Describe the late phase of atopic asthma
1) Inflammation that has occurred thus far now prompts epithelial cells in the lung to attract further eosinophils
a) promote further involvement of leukocytes and amplify inflammation
b) when this inflammatory response is oft repeated, structural changes occur in the lung
Describe the structural changes of atopic asthma:
1) Is there airway remodeling?
2) What are the other changes? Is there anything irreversible?
1) Includes hypertrophy of bronchial smooth muscle
2) Increased mucus glands + vasculature and deposition of epithelial collagen
-This all gives asthma and irreversible component in the late stage only
Asthma attacks:
1) What are they characterized by?
2) What will an X ray show?
3) How long does it last?
1) Severe dyspnea
-Bronchoconstriction and mucus plugging > wheeze and cough > air trapping in distal airspaces > hyperinflation of the lungs
2) X ray will be normal
3) This lasts from 1 to several hours
What is it called when asthma attacks don’t respond to therapy? What are the 3 characteristics?
Status asthmaticus:
1) Hypercapnia > acidosis
2) Hypoxia
3) Fatality
Bronchiectasis Pathology
1) What is it?
2) What is the end result of the destruction?
1) Permanent dilation of bronchi and bronchioles caused by destruction of SM and elastic tissue
2) Bronchi and bronchioles enlarge greatly, and the walls thicken
List and describe the 2 things that can be caused by permanent dilation of bronchi and bronchioles caused by destruction of SM and elastic tissue
1) Obstruction or chronic/necrotizing infection
-Foreign body / tumor > obstruction > superimposed infection
-CF > thick and viscous sputum > obstruction and recurrent infection
-Primary severe bacteria > obstructing purulent material
2) Inflammatory damage and fibrosis
-Bronchi and bronchioles enlarge greatly, and the walls thicken
Idiopathic Pulmonary Fibrosis:
1) What is it?
2) What is the etiology?
3) Describe 3 things its linked to
1) Disease of patchy, progressive bilateral interstitial fibrosis leading to restrictive disease
2) Etiology unclear; Genetic + environmental damage
3) Disease of alveolar epithelial cells, linked to heritable mutations in MUC5B and germline mutations in surfactant genes –both of which only expressed in the lung
-Also linked to loss of telomerase and cell senescence > only in older individuals (at least 50+)
-Some connection to GERD > repeated cellular injury
)Only very small portion of reflux patients develop this)
Pneumoconiosis:
1) Define it
2) What were its causes originally referred to as?
1) Accumulation of environmental particulate in the lung leading to disease
2) “Mineral dusts”: Coal, silica, asbestos
Pneumoconioses:
1) What are the 3 main causes?
2) What are the particle sizes?
1) Anthracosis (coal), Silicosis, Asbestosis
2)10 micrometers are too big to get to distal airway and become lodged in the bifrucations – removed through ciliary motion
0.5 micrometers pass to alveoli and move out from them
1-5 micrometers cause issues
Sarcoidosis:
1) What system does it involve?
2) Etiology?
3) What is the defining feature?
4) What occurs in 90% of cases?
1) Multisystemic disease
2) Unknown etiology
3) Defining feature is noncaseating granulomas in various tissues
4) Lung involvement in 90% of cases with formation of granulomas and interstitial fibrosis
Sarcoidosis:
1) What are 2 reasons for hypercalcemia?
2) What are some features of sarcoidosis?
1) Increased release 1,25-dihydroxy vitamin D
PTH related peptide (PTHrp) secreted by granulomas
2) Dry cough; peri-hilar LAD node enlargement; eyes (sicca syndrome-dry eyes, iritis, iridocyclitis); skin lesions (erythema nodosum & sub q nodules); visceral (liver)
Common causes of bacterial pneumonias in the community besides S. pneumonias include what?
H. influenzaeandM. catarrhalis(both associated with acute exacerbations of COPD),
S. aureus(usually secondary to viral respiratory infections)
K. pneumoniae(observed in chronic alcoholics),
P. aeruginosa(seen in individuals with cystic fibrosis, in burn victims, and in patients with neutropenia), and
L. pneumophila,seen particularly in organ transplant recipients.
Viral pneumoniasare characterized by what?
Respiratory distress out of proportion to the clinical and radiologic signs, and by inflammation that is predominantly confined to alveolar septa – interstitial space, with generally clear alveoli.
Common causes of viral pneumonia include what 3 things?
SARS Covid-2, influenza A and B, respiratory syncytial virus
Complications of acute pneumonias may occur in severe cases or in debilitated patients; give 5 examples
1) Pneumonia may extend to pleura, cause pleuritis, and heal as pleural fibrosis
2) Empyema: pus in pleural space
3) Abscess formation
4) Bronchiectasis from chronic lung infection
5) Interstitial fibrosis with cysts
TB Pathology:
1) What happens to get infected?
2) What causes primary TB? What does the body do?
3) What will happen next?
1) Lungs are sprayed with aerosolized TB
2) TB lands along the fissures and just under the exterior lung; macrophages address the invasion
3) They will have trouble dealing with mycobacterium, and thus wall it off w. caseating granuloma
Ghon focus > lung
Ghon focus + lymph node > Ghon Complex
Our initial battle with TB leads to 1 of 3 possibilities for the bacteria; what are they?
1) Death > TB dies
2) Dormancy > TB stops spreading
3) Division > TB replicates
-If option #2, the patient has “latent TB” and is without sx with normal CXR
1) What happens after you get primary TB?
2) What happens if a patient with latent TB is either reinfected or enters an immunosuppressed state? Explain
1) At this stage, your active immune system remembers TB and you will have antibodies this is how the PPD test works
2) The infxn can come back; Nnw they have “secondary TB”
-For reasons not fully understood, secondary TP usually occurs in the lung apices > cavitary lesions
-From here, TB can sometimes spread to the rest of the body
Know the Histologic Changes of Major Lung Cancer Types
(slide 82 picture)
Mnemonics for carcinomas are what?
“S” stands for “Sentral”
Squamous cell > scaley and obstructive
Adeno > grow slow
Small cell > small so it makes up for this with paraneoplastic disease
Cushing’s and SAIDH
Large cell, big deal because it grows fast
