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Pulm Block > Week 3- Gas Exchange > Flashcards

Week 3- Gas Exchange Flashcards

1
Q

Differentiate between hypoxia and hypoxemia

A

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

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2
Q

How to estimate the normal A-aDO2 based on age

A

(Age/4) +4

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3
Q

What are the five causes of hypoxemia and the two most common?

A
  1. low FiO2
  2. hypoventilation**
  3. diffusion impairment
  4. V/Q mismatch**
  5. shunt

**most common

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4
Q

What is the A-aDO2 gradient in the different causes of hypoxemia

A
  • Low FiO2: normal (PAO2 and Pa02 decrease the same amount)
  • Alveolar hypoventilation: normal (PAO2 and Pa02 decrease the same amount)
  • Diffusion impairment (high)
  • Shunt (high)
  • V/Q mismatch (high)
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5
Q

What is Fick’s law?

A

Diffusion proportional to:

  • area of diffusion
  • solubility of gas
  • partial pressure difference

Inversely proportional to

  • thickness of wall
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6
Q

What does the oxygen uptake look like in a normal and fibrotic lung alveolus?

A
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7
Q

What happens to oxygen uptake in alveolus during exercise (high cardiac output)?

A

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.

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8
Q

Is diffusion of CO2 a problem in fibrotic lungs the way diffusion of O2 is a problem?

A

No, because Co2 is much more soluble, only oxygen diffusion is affected.

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9
Q

Among hypoxemias that have high A-aDO2, which can be abolished by giving inspired oxygen?

A
  • Shunt cannot
  • V/Q mismatch can
  • Diffusion impairment can
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10
Q

When is V/Q high? When is V/Q low? How does the V/Q in one unit affect the PaCO2 and PaO2

A

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 (?)

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11
Q

Contrast physiologic and anatomic deadspace

A

Physiologic: the total deadspace (alveolar + anatomic)

Anatomic deadspace: the deadspace in the conducting airways

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12
Q

Define:

  • anatomic shunt
  • R to L shunt
  • Physiologic
  • Intrapulmonary

What do shunts do for gas exchange?

A

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**

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13
Q

What are some indications for pulmonary function testing?

A
  • respiratory symptoms (wheeze, cough, SOB)
  • monitoring chronic conditions like asthma or COPD
  • detecting lung changes as a patient ages, especially if they are smokers.
  • pre-operative assessment
  • baseline measurement before radiation
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14
Q

Specify how spirometry is performed.

A

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

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15
Q

Describe restrictive and obstructive ventilatory patterns on spirometry.

A

Obstructive:

  • low FEV1, FVC, FEV1:FVC

Restrictive

  • low FEV1, FVC
  • normal FEV1:FVC
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16
Q

What are different measures of expiratory flow? Which is best?

A
  • FEV1
  • PEF
  • FEV25
  • FEV75
  • FEV25-75

FEV1 is used most commonly. PEF is not very reliable because it is more effort dependent

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17
Q

What are the pros and cons of using PEF in a clinical setting?

A
  • simple device, allows asthma patients to self monitor
  • PEF is effort dependent, so in the clinic it is better to use FEV1
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18
Q

Briefly describe how diffusing capacity is measured

A
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19
Q

Briefly describe how total lung capacity can be measured

A
  • can use gas diffusion to measure lung volume (C1V1=C2V2)
  • can be done using a plethysomograph
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20
Q

How the inhalation of an infectious agent produces disease (pyogenic bacteria, virus, TB, fungi)

A
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21
Q

Where is the reservoir for TB?

What is the tranmission of TB?

A

In humans

Aerosols

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22
Q

Pathogenesis of TB

A
  • mycobacterium is inhaled, engluf by alveolar macrophage
  • macrophage tries to digest it, but can’t
  • mycobacterium proliferates
  • 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
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23
Q

Define primary TB and briefly describe its natural course.

A

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

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24
Q

Define Ghon complex

A

Ghon focus + lymph node involved

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25
How to detect TB in the sputum?
And AFB smear (Zielh Neelsen stain)
26
how does a ghon focus become visible on a radiograph?
Ghon focus--\> fibrosis--\> calcification
27
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.
28
What are some complications of secondary TB
* erosion of bronchi with cavitation * erosion of blood vessels with cavitation (hemoptysis) * miliary TB * isolated-organ TB
29
What MOTT (mycobacterium other than TB) is important in an AIDS patient?
mycobacterium avium complex if CD4 is low, patient may not have granulomas
30
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)
31
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)
32
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
33
What fungi could cause granulatomatous pneumonia in immunocompromised hosts
* aspergillus * candida * mucormycoses
34
pathology of fungal pneumonia in immunocompromised hosts
necrotizing pneumonia angioinvasion dissemination fungi manifest as hyphae, not spores
35
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: 1. resulting from inflammation and fibrosis OR 2. granuloma related
36
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
37
common interstitial lung diseases
sarcoidosis usual interstitial pneumonia (aka idiopathic pulmonary fibrosis, cryptogenic fibrosiing alveolitis) hypersensitivity pneumonitis pneumocosis
38
Common symptoms and signs (including radiological) of interstitial lung disease
* dyspnea * dry cough * clubbing sometimes * velcro rales * restrictive PFTs * bilateral basilar reticular markings on CXR \*\*usually occurs in middle-aged and elderly except with sarcoidosis\*\*
39
general etiologies of UIP
* idiopathic * collagen vascular disease * drug induced
40
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
41
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
42
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
43
Possible triggering injury in UIP
Environmental * cigarettes * metal dust * wood dust Infection * Hep C? * EBV? Radiation therapy?
44
Prognosis for UIP
* not good * median survival 3 yrs from onset of symptoms
45
treatment for UIP
not responsive to steroids O2 for quality of life, not prolongation of life
46
Environmental agents that are relevant to ILD
* smoke * asbestos * wood dust * metal dust * silicone etc...
47
Define ARDS
* acute respiratory distress syndrome * severe diffuse damage to the alveolar-capillary wall * clinically, rapid onset of life-threatening respiratory insufficiency
48
What is the etiology of ARDS?
Direct injury: * infection * irritants (e.g. oxygen toxicity) * gastric aspiration (infection by anaerobes?) Systemic conditions * septic shock * trauma associated shock
49
What are the phases of ARDS?
1. The early exudative phase. PMNs in alveoli, hyaline membranes 2. The organizing (healing) phase. Type 2 pneumocytes proliferate, collagen deposition, fibroblast proliferation.
50
How does endotoxin cause ARDS?
Induces release of TNF-alpha from alveolar macrophages. Inflammation! Edema, neutrophil activation (ROS, proteases, cytokines, complement C5a) Damage.
51
Pathology of ARDS (macroscopic and microscopic)
Macroscopic: * heavy, dense, red lungs Microscopic: * Early exudative: edema, cell necrosis, hylaine membranes * Organization (healing): lots of type 2 pneumocytes, fibrosis tissue
52
Define pneumonia
Generic term denoting inflammation of the pulmonary parenchyma.
53
Classifications of pneumonia
Can be classified by: Anatomy: * lobar * broncholobar * interstitial Clinical * community acquired * in immunocompromised host * hospital acquired * aspiration Etiology: * Bacterial * Viral * Other (fungal, pneumocystis, rickettsial, chlamydia, mycoplasmal)
54
What are some organisms that result in infectious pneumonia?
Bacterial * Haemophilus influenzae * Staph. aureus * strep. pneumoniae * anaerobes etc.. Viral * CMV * influenza Fungal * histoplasma * coccidiodes * cryptococcuse * blastomyces * aspergillus (immune compromised) * pneumocystis (immune compromised) * candida (immune compromised) * mucormycoses (immune compromised)
55
What are predisposing factors for pneumonia
cough suppresion * anesthetic, coma, neuromuscular disorder Impaired immunity * HIV, leukemia, chemo * impaired dust cell function Impaired clearance * smoking, underlying viral infection, immobile cilia Pulmonary edema General debility * malnourishment, post-op
56
Differentiate lobar and broncholobar pneumonia
Lobar * takes up a whole lobe * often bacterial (Strep pneumoniae) Broncholobar * patchy consolidation, usually confined to a few lobes
57
What are the stages of lobar pneumonia?
1. Congestion: edema +bacteria 2. Red hepatization: intra-alveolar neutrophils, RBCs 3. Grey hepatization: macrophages replace neutrophils 4. Resolution
58
Complications of lobar or bronchopulmonary pneumonia
* bacterial dissemination * lung abscess formation * empyema * death
59
Pathology of infective interstitial pneumonia
PMNs gather in interstitium rather than alveolus. Often has intraalveolar edema.
60
What kind of pneumonia does the immunocompromised host get?
* usual bacterial * mycobacterial * fungal * PCP * viral

Pulm Block (10 decks)

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