Differentiate between hypoxia and hypoxemia
hypoxia: a condition where all or part of the body doesn't receive adequete oxygen or is unable to use it for aerobic metabolism
hypoxemia: low oxygen in the arterial blood
How to estimate the normal A-aDO2 based on age
What are the five causes of hypoxemia and the two most common?
What is the A-aDO2 gradient in the different causes of hypoxemia
Low FiO2: normal (PAO2 and Pa02 decrease the same amount)
Alveolar hypoventilation: normal (PAO2 and Pa02 decrease the same amount)
Diffusion impairment (high)
V/Q mismatch (high)
What is Fick's law?
Diffusion proportional to:
- area of diffusion
- solubility of gas
- partial pressure difference
Inversely proportional to
- thickness of wall
What does the oxygen uptake look like in a normal and fibrotic lung alveolus?
What happens to oxygen uptake in alveolus during exercise (high cardiac output)?
Transit time decreases. In a healthy lung this is not a problem because there is lots of reserve time. There is not very much reserve time in the fibrotic lung, so increasing cardiac output will lead to hypoxemia.
Is diffusion of CO2 a problem in fibrotic lungs the way diffusion of O2 is a problem?
No, because Co2 is much more soluble, only oxygen diffusion is affected.
Among hypoxemias that have high A-aDO2, which can be abolished by giving inspired oxygen?
V/Q mismatch can
Diffusion impairment can
When is V/Q high? When is V/Q low? How does the V/Q in one unit affect the PaCO2 and PaO2
V/Q high: high ventilation, no perfusion--> contributes to high PAO2, no contribution to PaCO2 (?)
V/Q low: no ventilation, but high perfusion--> contributes to low PaO2, contributes to high PaCO2 (?)
Contrast physiologic and anatomic deadspace
Physiologic: the total deadspace (alveolar + anatomic)
Anatomic deadspace: the deadspace in the conducting airways
- anatomic shunt
- R to L shunt
What do shunts do for gas exchange?
When blood enters the circulation without having been in the lung capillaries first.
Pathologic (R to L shunt) e.g. tetralogy of Fallot
Physiologic e.g. thesbian veins, bronchial veins
Intrapulmonary would be a really low V/Q
**all limit gas exchange**
What are some indications for pulmonary function testing?
respiratory symptoms (wheeze, cough, SOB)
monitoring chronic conditions like asthma or COPD
detecting lung changes as a patient ages, especially if they are smokers.
baseline measurement before radiation
Specify how spirometry is performed.
A pneumotachograph instrument is used. The patient breathes in several tidal volumes and then a maximal inspiration followed by a maximal expiration.
From this can obtain lung volumes (except residual volume) and flow volume curves
Describe restrictive and obstructive ventilatory patterns on spirometry.
- low FEV1, FVC, FEV1:FVC
- low FEV1, FVC
- normal FEV1:FVC
What are different measures of expiratory flow? Which is best?
FEV1 is used most commonly. PEF is not very reliable because it is more effort dependent
What are the pros and cons of using PEF in a clinical setting?
simple device, allows asthma patients to self monitor
PEF is effort dependent, so in the clinic it is better to use FEV1
Briefly describe how diffusing capacity is measured
Briefly describe how total lung capacity can be measured
can use gas diffusion to measure lung volume (C1V1=C2V2)
can be done using a plethysomograph
How the inhalation of an infectious agent produces disease (pyogenic bacteria, virus, TB, fungi)
Where is the reservoir for TB?
What is the tranmission of TB?
Pathogenesis of TB
mycobacterium is inhaled, engluf by alveolar macrophage
macrophage tries to digest it, but can't
immune response--> monocytes, T cells
cell mediated immunity becomes hypersensitive to tuberculin antigen, and this contributes to tissue destruction
Ghon focus (pre-granuloma) develops, undergoes caseous necrosis
free bacteria or intracellular bacteria drain to lymph nodes where it all happens again
Define primary TB and briefly describe its natural course.
Primary tubrculosis develops in a previously unexposed person (usually found in lower lobe, or lower part of upper lobe). Usually pulmonary TB develops, and the mycobacterium spreads
Define Ghon complex
Ghon focus + lymph node involved
How to detect TB in the sputum?
And AFB smear (Zielh Neelsen stain)
how does a ghon focus become visible on a radiograph?
Ghon focus--> fibrosis--> calcification
Define secondary (reactivation TB). Where is it found usually?
Found in the upper lobes. Bacilli from the original infection get loose, usually when the host is immune compromised in some way.
What are some complications of secondary TB
erosion of bronchi with cavitation
erosion of blood vessels with cavitation (hemoptysis)
What MOTT (mycobacterium other than TB) is important in an AIDS patient?
mycobacterium avium complex
if CD4 is low, patient may not have granulomas
What is the macroscopic and microscopic appearance of TB
Macroscopic: caseous necrotic tissue
Microscopic: granuloma (lots of inflammatory cells, necrotic tissue, with giant cells and epitheloid histiocytes)
Which fungi could produce granulomatous pneumonia in immunocompetent host and where are they found
Blastomyces dermatidis (southeastern US)
Histoplasma capsulatum (Eastern US/southeast canada)
Coccidiodes immitis (Southwest US)
Cryptococcus neoformans (Bird droppings)
Cryptococcus gattii (Bird droppings: Vancouver island)
Pathology of fungal lung infections in immunocompetent hosts
similar to TB, except often have a solitary pulmonary nodule
need microbiology/histology to tell apart- in immunocompetent host fungi manifests as spores
What fungi could cause granulatomatous pneumonia in immunocompromised hosts
pathology of fungal pneumonia in immunocompromised hosts
fungi manifest as hyphae, not spores
define interstitial lung disease
disease involving the parenchyma of the lung distal to the small airways
more than 200 diseases are known to cause ILD
Can be classified as:
- resulting from inflammation and fibrosis OR
- granuloma related
What is sarcoidosis and how is the diagnosis made?
Sarcoidosis is a disease characterized by non-necrotizing granulomas
It is generally a diagnosis of exclusion
common interstitial lung diseases
usual interstitial pneumonia (aka idiopathic pulmonary fibrosis, cryptogenic fibrosiing alveolitis)
Common symptoms and signs (including radiological) of interstitial lung disease
bilateral basilar reticular markings on CXR
**usually occurs in middle-aged and elderly except with sarcoidosis**
general etiologies of UIP
collagen vascular disease
Pathogenesis of interstitial lung disease
epithelial cell injury
fibroblasts (granulation tissue) lays down collagen
epithelium grows over collagen
- the more this happens, the more alveoli collapse
- normal fibrinolytic mechanisms may be impaired with chronic ILD
- autoantibodies may contribute
- increased levels of profibrotic cytokines
- fibroblasts may behave abnormally
Pathogenesis of granulatomous interstitial lung disease, and main differential
something makes T-cells, macrophages accumulate in the parenchyma and become a big cluster of cells known as a granuloma
main differential: sarcoidosis and hypersensitivity pneumonitis
What is the PFT pattern for ILD
Follows a restrictive pattern:
- small volumes (FVC, FEV1, TLC)
- flows preserved or increased
- compliance decreased
- diffusing capacity decreased
Possible triggering injury in UIP
- metal dust
- wood dust
- Hep C?
Prognosis for UIP
median survival 3 yrs from onset of symptoms
treatment for UIP
not responsive to steroids
O2 for quality of life, not prolongation of life
Environmental agents that are relevant to ILD
acute respiratory distress syndrome
severe diffuse damage to the alveolar-capillary wall
clinically, rapid onset of life-threatening respiratory insufficiency
What is the etiology of ARDS?
- irritants (e.g. oxygen toxicity)
- gastric aspiration (infection by anaerobes?)
- septic shock
- trauma associated shock
What are the phases of ARDS?
The early exudative phase. PMNs in alveoli, hyaline membranes
The organizing (healing) phase. Type 2 pneumocytes proliferate, collagen deposition, fibroblast proliferation.
How does endotoxin cause ARDS?
Induces release of TNF-alpha from alveolar macrophages. Inflammation!
Edema, neutrophil activation (ROS, proteases, cytokines, complement C5a)
Pathology of ARDS (macroscopic and microscopic)
- heavy, dense, red lungs
- Early exudative: edema, cell necrosis, hylaine membranes
- Organization (healing): lots of type 2 pneumocytes, fibrosis tissue
Generic term denoting inflammation of the pulmonary parenchyma.
Classifications of pneumonia
Can be classified by:
- community acquired
- in immunocompromised host
- hospital acquired
- Other (fungal, pneumocystis, rickettsial, chlamydia, mycoplasmal)
What are some organisms that result in infectious pneumonia?
- Haemophilus influenzae
- Staph. aureus
- strep. pneumoniae
- anaerobes etc..
- aspergillus (immune compromised)
- pneumocystis (immune compromised)
- candida (immune compromised)
- mucormycoses (immune compromised)
What are predisposing factors for pneumonia
- anesthetic, coma, neuromuscular disorder
- HIV, leukemia, chemo
- impaired dust cell function
- smoking, underlying viral infection, immobile cilia
- malnourishment, post-op
Differentiate lobar and broncholobar pneumonia
- takes up a whole lobe
- often bacterial (Strep pneumoniae)
- patchy consolidation, usually confined to a few lobes
What are the stages of lobar pneumonia?
Congestion: edema +bacteria
Red hepatization: intra-alveolar neutrophils, RBCs
Grey hepatization: macrophages replace neutrophils
Complications of lobar or bronchopulmonary pneumonia
lung abscess formation
Pathology of infective interstitial pneumonia
PMNs gather in interstitium rather than alveolus. Often has intraalveolar edema.
What kind of pneumonia does the immunocompromised host get?